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{{Short description|Beta blocker medication}} |
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{{refimprove|date=October 2010}} |
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{{Use dmy dates|date=January 2024}} |
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{{Drugbox |
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{{cs1 config|name-list-style=vanc|display-authors=6}} |
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| verifiedrevid = 443402376 |
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{{Infobox drug |
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| IUPAC_name = (''RS'')-2-{4-phenyl}acetamide |
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| Watchedfields = changed |
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| image = (±)-Atenolol Enantiomers Structural Formulae.png |
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| verifiedrevid = 458476745 |
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| width = 275 |
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| image = Atenolol structure.svg |
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| width = 200 |
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| alt = |
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| image2 = Atenolol_3d_structure.png |
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| image2 = Atenolol_3d_structure.png |
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| width2 = 275 |
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| width2 = 200 |
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| alt2 = |
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| imagename = 1 : 1 mixture (racemate) |
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| chirality = ] |
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| drug_name = Atenolol |
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<!--Clinical data--> |
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<!-- Clinical data --> |
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| tradename = Tenormin |
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| tradename = Tenormin, others |
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| Drugs.com = {{drugs.com|monograph|atenolol}} |
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| Drugs.com = {{drugs.com|monograph|atenolol}} |
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| MedlinePlus = a684031 |
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| MedlinePlus = a684031 |
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| licence_US = Atenolol |
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| DailyMedID = Atenolol |
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| pregnancy_AU = C |
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| pregnancy_AU = C |
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| routes_of_administration = ], ] |
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| pregnancy_US = D |
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| class = ] ] ] |
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| ATC_prefix = C07 |
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| ATC_suffix = AB03 |
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<!-- Legal status --> |
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| legal_AU = S4 |
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| legal_status = Rx-only |
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| legal_status = Rx-only |
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| routes_of_administration = Oral or ] |
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<!--Pharmacokinetic data--> |
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<!-- Pharmacokinetic data --> |
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| bioavailability = 50–60%<ref name="WadworthMurdochBrogden1991" /><ref name="HeelBrogdenSpeight1979" /> |
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| bioavailability = 40-50% |
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| protein_bound = 6–16%<ref name="TenorminLabel">{{cite web |title=DailyMed - TENORMIN- atenolol tablet|website=DailyMed |date=30 June 2021|url=https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=746db603-a6e1-4dc3-c2d8-92314419098c|access-date=20 November 2023|archive-url=https://web.archive.org/web/20220127140640/https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=746db603-a6e1-4dc3-c2d8-92314419098c|archive-date=27 January 2022|url-status=live}}</ref> |
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| protein_bound = 6-16% |
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| metabolism = Minimal (~5%)<ref name="TenorminLabel" /><ref name="BroddeKroemer2003" /><ref name="KirchGörg1982" /> |
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| metabolism = ] <10% |
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| metabolites = • Hydroxyatenolol<ref name="HeelBrogdenSpeight1979" /><br />• Atenolol glucuronide<ref name="HeelBrogdenSpeight1979" /> |
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| elimination_half-life = 6-7hours |
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| onset = {{Abbrlink|IV|Intravenous injection}}: <5 minutes<ref name="TenorminLabel" /><br />]: <1 hour<ref name="TenorminLabel" /> |
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| excretion = ]<br />] (In lactiferous females) |
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| elimination_half-life = 6–7 hours<ref name="TenorminLabel" /> |
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| duration_of_action = >24 hours<ref name="TenorminLabel" /> |
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| excretion = ]: ] (40–50%), ] (50%)<ref name="HeelBrogdenSpeight1979" /><ref name="TenorminLabel" /><br />{{Abbrlink|IV|Intravenous injection}}: urine (85–100%), feces (10%)<ref name="HeelBrogdenSpeight1979" /><ref name="TenorminLabel" /> |
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<!--Identifiers--> |
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<!-- Identifiers --> |
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| CASNo_Ref = {{cascite|correct|CAS}} |
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| CAS_number_Ref = {{cascite|correct|??}} |
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| CAS_number = 29122-68-7 |
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| CAS_number = 29122-68-7 |
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| ATC_prefix = C07 |
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| ATC_suffix = AB03 |
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| PubChem = 2249 |
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| PubChem = 2249 |
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| IUPHAR_ligand = 548 |
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| IUPHAR_ligand = 548 |
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| ChEMBL_Ref = {{ebicite|correct|EBI}} |
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| ChEMBL_Ref = {{ebicite|correct|EBI}} |
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| ChEMBL = 24 |
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| ChEMBL = 24 |
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| synonyms = ICI-66082; ICI66082 |
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<!--Chemical data--> |
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<!-- Chemical data --> |
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| IUPAC_name = (''RS'')-2-<nowiki/>{4-phenyl}acetamide |
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| C=14 | H=22 | N=2 | O=3 |
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| C=14 | H=22 | N=2 | O=3 |
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| molecular_weight = 266.336 g/mol |
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| smiles = O=C(N)Cc1ccc(OCC(O)CNC(C)C)cc1 |
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| SMILES = O=C(N)Cc1ccc(cc1)OCC(O)CNC(C)C |
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| InChI = 1/C14H22N2O3/c1-10(2)16-8-12(17)9-19-13-5-3-11(4-6-13)7-14(15)18/h3-6,10,12,16-17H,7-9H2,1-2H3,(H2,15,18) |
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| InChIKey = METKIMKYRPQLGS-UHFFFAOYAT |
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| StdInChI_Ref = {{stdinchicite|correct|chemspider}} |
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| StdInChI_Ref = {{stdinchicite|correct|chemspider}} |
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| StdInChI = 1S/C14H22N2O3/c1-10(2)16-8-12(17)9-19-13-5-3-11(4-6-13)7-14(15)18/h3-6,10,12,16-17H,7-9H2,1-2H3,(H2,15,18) |
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| StdInChI = 1S/C14H22N2O3/c1-10(2)16-8-12(17)9-19-13-5-3-11(4-6-13)7-14(15)18/h3-6,10,12,16-17H,7-9H2,1-2H3,(H2,15,18) |
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| StdInChIKey = METKIMKYRPQLGS-UHFFFAOYSA-N |
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| StdInChIKey = METKIMKYRPQLGS-UHFFFAOYSA-N |
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}} |
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}} |
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<!-- Definition and symptoms --> |
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'''Atenolol''' is a selective ] ], a ] belonging to the group of ]s (sometimes written β-blockers), a class of drugs used primarily in ]s. Introduced in 1976, atenolol was developed as a replacement for ] in the treatment of ]. The chemical works by slowing down the heart and reducing its workload. Unlike ], atenolol does not pass through the blood-brain barrier thus avoiding various ] side effects.<ref name="BBB">{{cite journal |author=Agon P, Goethals P, Van Haver D, Kaufman JM |title=Permeability of the blood-brain barrier for atenolol studied by positron emission tomography |journal=J. Pharm. Pharmacol. |volume=43 |issue=8 |pages=597–600 |year=1991 |month=August |pmid=1681079 |doi= |url= }}</ref> |
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'''Atenolol''' is a ] medication primarily used to treat ] and ].<ref name=AHFS2018/> Although used to treat high blood pressure, it does not seem to improve ] in those with the condition.<ref>{{cite journal | vauthors = Tomiyama H, Yamashina A | title = Beta-Blockers in the Management of Hypertension and/or Chronic Kidney Disease | journal = International Journal of Hypertension | volume = 2014 | pages = 919256 | year = 2014 | pmid = 24672712 | pmc = 3941231 | doi = 10.1155/2014/919256 | doi-access = free }}</ref><ref>{{cite journal | vauthors = DiNicolantonio JJ, Fares H, Niazi AK, Chatterjee S, D'Ascenzo F, Cerrato E, Biondi-Zoccai G, Lavie CJ, Bell DS, O'Keefe JH | title = β-Blockers in hypertension, diabetes, heart failure and acute myocardial infarction: a review of the literature | journal = Open Heart | volume = 2 | issue = 1 | pages = e000230 | year = 2015 | pmid = 25821584 | pmc = 4371808 | doi = 10.1136/openhrt-2014-000230 }}</ref> Other uses include the prevention of ] and treatment of certain ]s.<ref name=AHFS2018/><ref name=BNF76>{{cite book|title=British national formulary : BNF 76|date=2018|publisher=Pharmaceutical Press|isbn=9780857113382|pages=151–153|edition=76}}</ref> It is taken ] (by mouth) or by ] (injection into a vein).<ref name=AHFS2018/><ref name=BNF76/> It can also be used with other ]s.<ref name=BNF76/> |
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<!-- Side effects and mechanism --> |
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Atenolol is one of the most widely used β-blockers in the ] and was once the first-line treatment for hypertension. The role for β-blockers in hypertension was downgraded in June 2006 in the United Kingdom to fourth-line, as they perform less appropriately or effectively than newer drugs, particularly in the elderly. Some evidence suggests that even in normal doses the most frequently used β-blockers carry an unacceptable risk of provoking ].<ref name="NHSnews">{{cite web | author= Sheetal Ladva | title=Updated NICE guideline on the management of hypertension in adults in primary care | url=http://www.nelm.nhs.uk/en/NeLM-Area/Evidence/Guidelines/Updated-NICE-guideline-on-the-management-of-hypertension-in-adults-in-primary-care/ | date=2006-06-30 | publisher=] | accessdate=2009-02-03}}</ref> |
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Common ]s include ], ], ], ], and ].<ref name=AHFS2018/> Other serious side effects include ].<ref name=AHFS2018/> Use is not recommended during ]<ref name=AHFS2018/> and alternative drugs are preferred when ].<ref>{{cite web |title=Atenolol use while Breastfeeding |url=https://www.drugs.com/breastfeeding/atenolol.html |website=Drugs.com |access-date=23 December 2018 |archive-date=23 December 2018 |archive-url=https://web.archive.org/web/20181223121344/https://www.drugs.com/breastfeeding/atenolol.html |url-status=live }}</ref> It works by blocking ]s in the ], thus decreasing ], ]s, and ].<ref name=AHFS2018/> |
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<!-- History and culture --> |
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Atenolol was patented in 1969 and approved for medical use in 1975.<ref name=Fis2006>{{cite book| vauthors = Fischer J, Ganellin CR |title=Analogue-based Drug Discovery|date=2006|publisher=John Wiley & Sons|isbn=9783527607495|page=461|url=https://books.google.com/books?id=FjKfqkaKkAAC&pg=PA461}}</ref> It is on the ].<ref name="WHO22nd">{{cite book | vauthors = ((World Health Organization)) | title = World Health Organization model list of essential medicines: 22nd list (2021) | year = 2021 | hdl = 10665/345533 | author-link = World Health Organization | publisher = World Health Organization | location = Geneva | id = WHO/MHP/HPS/EML/2021.02 | hdl-access=free }}</ref> It is available as a ].<ref name=AHFS2018>{{cite web |title=Atenolol Monograph for Professionals |url=https://www.drugs.com/monograph/atenolol.html |website=Drugs.com |publisher=AHFS |access-date=23 December 2018 |archive-date=18 April 2019 |archive-url=https://web.archive.org/web/20190418043029/https://www.drugs.com/monograph/atenolol.html |url-status=live }}</ref> In 2022, it was the 63rd most commonly prescribed medication in the United States, with more than 10{{nbsp}}million prescriptions.<ref>{{cite web | title=The Top 300 of 2022 | url=https://clincalc.com/DrugStats/Top300Drugs.aspx | website=ClinCalc | access-date=30 August 2024 | archive-date=30 August 2024 | archive-url=https://web.archive.org/web/20240830202410/https://clincalc.com/DrugStats/Top300Drugs.aspx | url-status=live }}</ref><ref>{{cite web | title = Atenolol Drug Usage Statistics, United States, 2013 - 2022 | website = ClinCalc | url = https://clincalc.com/DrugStats/Drugs/Atenolol | access-date = 30 August 2024 }}</ref> |
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==Medical uses== |
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==Medical uses== |
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Atenolol is used for a number of conditions including: ], ], ], ], ], ], prevention of ], and the symptoms of ].<ref name=AHFS>{{cite web|title=Atenolol|url=http://www.drugs.com/monograph/atenolol.html|work=The American Society of Health-System Pharmacists|accessdate=3 April 2011}}</ref> |
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Atenolol is used for a number of conditions including ],<ref name="Rehman Sanchez Shah 2021 p. ">{{cite book | vauthors = Rehman B, Sanchez DP, Shah S | chapter = Atenolol | title = StatPearls | publisher=StatPearls Publishing | publication-place=Treasure Island (FL) | year=2021 | pmid=30969666 | chapter-url=http://www.ncbi.nlm.nih.gov/books/NBK539844/ | access-date=5 September 2021 | page= | archive-date=10 October 2022 | archive-url=https://web.archive.org/web/20221010053047/https://www.ncbi.nlm.nih.gov/books/NBK539844/ | url-status=live }}</ref> ], ], ], ], ], ], ], and the symptoms of ].<ref name=AHFS>{{cite web|title=Atenolol|url=https://www.drugs.com/monograph/atenolol.html|work=The American Society of Health-System Pharmacists|access-date=8 May 2018|archive-date=18 April 2019|archive-url=https://web.archive.org/web/20190418043029/https://www.drugs.com/monograph/atenolol.html|url-status=live}}</ref> |
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The role for β-blockers in general in hypertension was downgraded in June 2006 in the United Kingdom, and later in the United States, as they are less appropriate than other agents such as ], ]s, ] diuretics and ], particularly in the elderly.<ref name="Cochrane2017">{{cite journal | vauthors = Wiysonge CS, Bradley HA, Volmink J, Mayosi BM, Opie LH | title = Beta-blockers for hypertension | journal = The Cochrane Database of Systematic Reviews | volume = 1 | pages = CD002003 | date = January 2017 | issue = 1 | pmid = 28107561 | pmc = 5369873 | doi = 10.1002/14651858.CD002003.pub5 | quote = Further research should be of high quality and should explore whether there are differences between different subtypes of beta-blockers or whether beta-blockers have differential effects on younger and older people Beta-blockers were not as good at preventing the number of deaths, strokes, and heart attacks as other classes of medicines such as diuretics, calcium-channel blockers, and renin-angiotensin system inhibitors. Most of these findings come from one type of beta-blocker called atenolol. However, beta-blockers are a diverse group of medicines with different properties, and we need more well-conducted research in this area." (p. 2-3) }}</ref><ref name="NHSnews">{{cite web| vauthors = Ladva S |date=28 June 2006|title=NICE and BHS launch updated hypertension guideline|url=http://www.nelm.nhs.uk/Record%20Viewing/viewRecord.aspx?id=|url-status=dead|archive-url=https://archive.today/20080511034248/http://www.nelm.nhs.uk/Record%20Viewing/viewRecord.aspx?id=567178|archive-date=11 May 2008|access-date=19 August 2012|publisher=]}}</ref><ref name="Cruickshank2007">{{cite journal | vauthors = Cruickshank JM | title = Are we misunderstanding beta-blockers | journal = International Journal of Cardiology | volume = 120 | issue = 1 | pages = 10–27 | date = August 2007 | pmid = 17433471 | doi = 10.1016/j.ijcard.2007.01.069 }}</ref> |
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It is also used to treat the symptoms of ], until ] medication can take effect. |
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===Available forms=== |
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Due to its hydrophilic properties, the drug is less suitable in ] prophylaxis compared to propranolol, because, for this indication, atenolol would have to reach the brain in high concentrations, which is not the case.{{Citation needed|date=April 2011}} |
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Atenolol is available in the form of 25, 50, and 100{{nbsp}}mg ] ]s.<ref name="Drugs@FDA">{{cite web | title=Drugs@FDA: FDA-Approved Drugs | website=accessdata.fda.gov | url=https://www.accessdata.fda.gov/scripts/cder/daf/index.cfm | access-date=8 July 2024}}</ref><ref name="TenorminLabel" /> It is also available in the form of oral tablets containing a ] of 50 or 100{{nbsp}}mg atenolol and 50{{nbsp}}mg ].<ref name="Drugs@FDA" /> Atenolol was previously available in a 0.5{{nbsp}}mg/mL solution for ] as well, but this formulation was discontinued.<ref name="Drugs@FDA" /> |
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==Side effects== |
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===Combination treatment of hypertension=== |
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{{See also|Beta blocker}} |
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If atenolol alone fails to control arterial hypertension, the drug can be combined with a diuretic (e.g. with ] in ]) and/or a vasodilator (], or in severe cases ]). Central alpha-agonists (e.g. ]), ]s or ]s such as ] can also be given additionally. Exert caution with calcium-antagonists of the ]-type (non-], see also ]) as adjunct therapy because of additional negative impact on the muscular strength of the heart. Use of calcium-antagonists of the ]-type is controversial. |
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Hypertension treated with a β-blocker such as atenolol, alone or in conjunction with a thiazide diuretic, is associated with a higher incidence of new onset type 2 diabetes mellitus compared to those treated with an ACE inhibitor or angiotensin receptor blocker.<ref>{{cite journal | vauthors = Lindholm LH, Ibsen H, Borch-Johnsen K, Olsen MH, Wachtell K, Dahlöf B, Devereux RB, Beevers G, de Faire U, Fyhrquist F, Julius S, Kjeldsen SE, Kristianson K, Lederballe-Pedersen O, Nieminen MS, Omvik P, Oparil S, Wedel H, Aurup P, Edelman JM, Snapinn S | title = Risk of new-onset diabetes in the Losartan Intervention For Endpoint reduction in hypertension study | journal = Journal of Hypertension | volume = 20 | issue = 9 | pages = 1879–86 | date = September 2002 | pmid = 12195132 | doi = 10.1097/00004872-200209000-00035 | s2cid = 23613019 }}</ref><ref>{{cite journal | vauthors = Elliott WJ, Meyer PM | title = Incident diabetes in clinical trials of antihypertensive drugs: a network meta-analysis | journal = Lancet | volume = 369 | issue = 9557 | pages = 201–7 | date = January 2007 | pmid = 17240286 | doi = 10.1016/s0140-6736(07)60108-1 | s2cid = 37044384 }}</ref> |
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==Contraindications== |
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*] (pulse less than 50 bpm) |
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*] |
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*] (may cause broncho-constriction), although unlikely as atenolol is cardioselective |
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*symptomatic hypotension (blood pressure of less than 90/60 mm Hg with dizziness, vertigo etc.) |
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*angina of the ] type (vasospastic angina) |
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*] (a severe condition with a more acidic blood than normal) |
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*severe disorders in peripheral arterial circulation |
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*AV-Blockage of second and third degree (a particular form of ]) |
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*acutely decompensated congestive heart failure (symptoms may be fluid retention with peripheral ] and/or abdominal fluid retention (ascites), and/or lung edema) |
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*] (a particular form of arrhythmia) |
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*hypersensitivity and/or ] to atenolol |
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*] (a rare type of tumor of the adrenal glands) |
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Caution: patients with preexisting bronchial asthma |
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β-blockers, of which atenolol is mainly studied, provides weaker protection against ] and mortality in patients over 60 years old compared to other antihypertensive medications.<ref>{{cite journal| vauthors = Lindholm LH, Carlberg B, Samuelsson O |date=October 2005|title=Should β blockers remain first choice in the treatment of primary hypertension? A meta-analysis |journal=The Lancet|language=en|volume=366|issue=9496|pages=1545–1553|doi=10.1016/S0140-6736(05)67573-3|pmid=16257341|s2cid=34364430}}</ref><ref>{{cite journal | vauthors = Khan N, McAlister FA | title = Re-examining the efficacy of beta-blockers for the treatment of hypertension: a meta-analysis | journal = CMAJ | volume = 174 | issue = 12 | pages = 1737–42 | date = June 2006 | pmid = 16754904 | pmc = 1471831 | doi = 10.1503/cmaj.060110 }}</ref><ref>{{cite journal | vauthors = Kuyper LM, Khan NA | title = Atenolol vs nonatenolol β-blockers for the treatment of hypertension: a meta-analysis | language = English | journal = The Canadian Journal of Cardiology | volume = 30 | issue = 5 Suppl | pages = S47-53 | date = May 2014 | pmid = 24750981 | doi = 10.1016/j.cjca.2014.01.006 | doi-access = free }}</ref><ref name="Cochrane2017" /> ]s may be associated with better cardiovascular and cerebrovascular outcomes than β-blockers in the elderly.<ref name="pmid15530629">{{cite journal | vauthors = Messerli FH, Grossman E, Goldbourt U | title = Are beta-blockers efficacious as first-line therapy for hypertension in the elderly? A systematic review | journal = JAMA | volume = 279 | issue = 23 | pages = 1903–7 | date = June 1998 | pmid = 9634263 | doi = 10.1001/jama.279.23.1903 }}</ref> |
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Caution: only if clearly needed during ], as atenolol may retard fetal growth and possibly cause other abnormalities. |
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Rarely, atenolol has been associated with induction of acute ].<ref name="KellerFrishman2003">{{cite journal | vauthors = Keller S, Frishman WH | title = Neuropsychiatric effects of cardiovascular drug therapy | journal = Cardiol Rev | volume = 11 | issue = 2 | pages = 73–93 | date = 2003 | pmid = 12620132 | doi = 10.1097/01.CRD.0000053453.89776.2D | url = }}</ref><ref name="WadworthMurdochBrogden1991">{{cite journal | vauthors = Wadworth AN, Murdoch D, Brogden RN | title = Atenolol. A reappraisal of its pharmacological properties and therapeutic use in cardiovascular disorders | journal = Drugs | volume = 42 | issue = 3 | pages = 468–510 | date = September 1991 | pmid = 1720383 | doi = 10.2165/00003495-199142030-00007 | url = }}</ref><ref name="Arber1988">{{cite journal | vauthors = Arber N | title = Delirium induced by atenolol | journal = BMJ | volume = 297 | issue = 6655 | pages = 1048 | date = October 1988 | pmid = 3142623 | pmc = 1834788 | doi = 10.1136/bmj.297.6655.1048-b | url = }}</ref> |
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==Side effects== |
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{{see also|Beta blocker}} |
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Atenolol causes significantly fewer central nervous system side effects (depression, nightmares) and fewer bronchospastic reactions,{{clarify|date=October 2010}} both due to its particular pharmacologic profile.{{Citation needed|date=October 2010}} |
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==Overdose== |
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It was the main β-blocker identified as carrying a higher risk of provoking ], leading to its downgrading in the United Kingdom in June 2006 to fourth-line agent in the management of hypertension.<ref name="NHSnews"/> |
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Symptoms of ] are due to excessive pharmacodynamic actions on β<sub>1</sub> and also β<sub>2</sub>-receptors. These include ] (slow heartbeat), severe ] with ], acute ], ] and bronchospastic reactions. Treatment is largely symptomatic. Hospitalization and intensive monitoring is indicated. ] is useful to absorb the drug. ] will counteract bradycardia, ] helps with hypoglycemia, ] can be given against hypotension and the inhalation of a β<sub>2</sub>-mimetic such as ] or ] will terminate bronchospasms. Blood or plasma atenolol concentrations may be measured to confirm a diagnosis of poisoning in hospitalized patients or to assist in a medicolegal death investigation. Plasma levels are usually less than 3 mg/L during therapeutic administration, but can range from 3–30 mg/L in overdose victims.<ref>{{cite journal | vauthors = DeLima LG, Kharasch ED, Butler S | title = Successful pharmacologic treatment of massive atenolol overdose: sequential hemodynamics and plasma atenolol concentrations | journal = Anesthesiology | volume = 83 | issue = 1 | pages = 204–7 | date = July 1995 | pmid = 7605000 | doi = 10.1097/00000542-199507000-00025 }}</ref><ref>{{cite book| vauthors = Baselt R |title=Disposition of Toxic Drugs and Chemicals in Man|edition=8th|publisher=Biomedical Publications|location=Foster City, Calif.|year=2008|pages=116–117}}</ref> |
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==Interactions== |
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In addition, β-blockers blunt the usual sympathetic nervous system response to hypoglycemia (i.e. sweating, agitation, tachycardia). These drugs therefore have an ability to mask a dangerously low blood sugar, which further decreases their safety and utility in diabetic patients. |
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] with atenolol include ]s like ], ]s, ], ], ], ]s like ], and ].<ref name="Atenolol-Label">{{cite web | title=TENORMIN® (atenolol) Tablets Drug Label | date = December 2023 | publisher = Food and Drug Administration | url=https://www.accessdata.fda.gov/drugsatfda_docs/label/2023/018240s047lbl.pdf | access-date=8 July 2024}}</ref> Most of these interactions involve either additive cardiovascular effects or reduction of atenolol's effects.<ref name="Atenolol-Label" /> |
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Atenolol is mainly ] ] without being ] by the ] or by ] ]s.<ref name="Atenolol-Label" /><ref name="BroddeKroemer2003">{{cite journal | vauthors = Brodde OE, Kroemer HK | title = Drug-drug interactions of beta-adrenoceptor blockers | journal = Arzneimittelforschung | volume = 53 | issue = 12 | pages = 814–822 | date = 2003 | pmid = 14732961 | doi = 10.1055/s-0031-1299835 | url = | quote = Atenolol is only minimally, if at all, metabolized and renally excreted in mostly unchanged form; thus an interaction with drugs that interfere with the hepatic metabolism is not to be expected. It is also very unlikely that the genetic polymorphisms of the CYP-family might affect the pharmacokinetics of atenolol. In fact it has been shown that plasma concentrations of nonmetabolized atenolol was not significantly different between “extensive” and “poor debrisoquine metabolizers” – in contrast to the plasma concentrations of metoprolol that were significantly increased in “poor metabolizers” (Dayer et al. 1985, Lewis et al. 1985). Furthermore, in healthy volunteers cimetidine (CAS 70059- 30-2) did not affect plasma concentrations of atenolol but significantly increased plasma concentrations of metoprolol or propranolol (Kirch et al. 1981).}}</ref><ref name="Scheen2011">{{cite journal | vauthors = Scheen AJ | title = Cytochrome P450-mediated cardiovascular drug interactions | journal = Expert Opin Drug Metab Toxicol | volume = 7 | issue = 9 | pages = 1065–1082 | date = September 2011 | pmid = 21810031 | doi = 10.1517/17425255.2011.586337 | url = | quote = β-Blockers still represent widely prescribed drugs as they cover a wide spectrum of CV indications. Obviously, it is not trivial which β-blocker to choose as they differ both with regard to their PD and PK profiles . It is well known when comparing the characteristics of atenolol, bisoprolol, metoprolol (each β-1 selective) and carvedilol (β-1 and β-2 nonselective). Among these β-blockers, atenolol is mainly eliminated by renal excretion; bisoprolol is in part excreted as parent compound via the renal route (50%); the other 50% are hepatically metabolized; whereas metoprolol and carvedilol are metabolized by CYP2D6. DDIs are mainly observed with those β-blockers that are metabolized via CYP enzymes. However, it should be emphasized that, in general, β-blockers are well-tolerated safe drugs with a large therapeutic index .}}</ref> As a result, it has little or no potential for cytochrome P450-related drug interactions, for instance with ]s and ]s of these enzymes.<ref name="BroddeKroemer2003" /><ref name="Scheen2011" /> Accordingly, the broad/] cytochrome P450 inhibitor ] had no effect on atenolol levels, whereas cimetidine has been found to significantly increase ] and ] levels.<ref name="BroddeKroemer2003" /> |
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Side effects include: |
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*], ] |
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*dry mouth |
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*dizziness or faintness (especially cases of ]) |
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*cold extremities |
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*hair loss |
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*impotence |
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*] |
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*depression |
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*confusion |
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*insomnia, nightmares |
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*fatigue, weakness or lack of energy |
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These side effects may or may not be experienced, but if they are, you should notify your doctor. |
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Beta blockers like atenolol can reduce or block the ] effects of ]s and ]s, such as ] and ].<ref name="RichardsAlbertsonDerlet2015">{{cite journal | vauthors = Richards JR, Albertson TE, Derlet RW, Lange RA, Olson KR, Horowitz BZ | title = Treatment of toxicity from amphetamines, related derivatives, and analogues: a systematic clinical review | journal = Drug Alcohol Depend | volume = 150 | issue = | pages = 1–13 | date = May 2015 | pmid = 25724076 | doi = 10.1016/j.drugalcdep.2015.01.040 | url = }}</ref><ref name="VetterEliaErickson2008">{{cite journal | vauthors = Vetter VL, Elia J, Erickson C, Berger S, Blum N, Uzark K, Webb CL | title = Cardiovascular monitoring of children and adolescents with heart disease receiving medications for attention deficit/hyperactivity disorder : a scientific statement from the American Heart Association Council on Cardiovascular Disease in the Young Congenital Cardiac Defects Committee and the Council on Cardiovascular Nursing | journal = Circulation | volume = 117 | issue = 18 | pages = 2407–2423 | date = May 2008 | pmid = 18427125 | doi = 10.1161/CIRCULATIONAHA.107.189473 | url = | quote = Amphetamines (Adderall, Dexedrine): Electrophysiological Effects of Amphetamines: Amphetamines have been associated with tachyarrhythmias and sudden death.113–115 Many of the electrophysiological effects of amphetamines may be initiated by the release of norepinephrine stores from presynaptic vesicles and blocking of norepinephrine reuptake.116,117 In addition, amphetamines are potent blockers of dopamine uptake and strong central nervous system stimulants. Dopaminergic Effects of Amphetamines: In addition to the β-agonist effects of amphetamines, the dopamine receptors D1 and D2 contribute to the cardiovascular effects of methamphetamine by producing a pressor response accounting for the increase in blood pressure. The D1 receptor also is involved in mediating the positive tachycardic effects of methamphetamine.117}}</ref><ref name="SchindlerZhengTella1992">{{cite journal | vauthors = Schindler CW, Zheng JW, Tella SR, Goldberg SR | title = Pharmacological mechanisms in the cardiovascular effects of methamphetamine in conscious squirrel monkeys | journal = Pharmacol Biochem Behav | volume = 42 | issue = 4 | pages = 791–796 | date = August 1992 | pmid = 1325059 | doi = 10.1016/0091-3057(92)90031-a | url = | doi-access = free }}</ref><ref name="MoresCampiaNavarra1999">{{cite journal | vauthors = Mores N, Campia U, Navarra P, Cardillo C, Preziosi P | title = No cardiovascular effects of single-dose pseudoephedrine in patients with essential hypertension treated with beta-blockers | journal = Eur J Clin Pharmacol | volume = 55 | issue = 4 | pages = 251–254 | date = June 1999 | pmid = 10424315 | doi = 10.1007/s002280050624 | url = }}</ref><ref name="HassanGunaidElKhally2005">{{cite journal | vauthors = Hassan NA, Gunaid AA, El-Khally FM, Al-Noami MY, Murray-Lyon IM | title = Khat chewing and arterial blood pressure. A randomized controlled clinical trial of alpha-1 and selective beta-1 adrenoceptor blockade | journal = Saudi Med J | volume = 26 | issue = 4 | pages = 537–541 | date = April 2005 | pmid = 15900355 | doi = | url = }}</ref><ref name="OConnellGross1990">{{cite journal | vauthors = O'Connell MB, Gross CR | title = The effect of single-dose phenylpropanolamine on blood pressure in patients with hypertension controlled by beta blockers | journal = Pharmacotherapy | volume = 10 | issue = 2 | pages = 85–91 | date = 1990 | pmid = 2349137 | doi = 10.1002/j.1875-9114.1990.tb02554.x| url = }}</ref><ref name="OConnellGross1991">{{cite journal | vauthors = O'Connell MB, Gross CR | title = The effect of multiple doses of phenylpropanolamine on the blood pressure of patients whose hypertension was controlled with beta blockers | journal = Pharmacotherapy | volume = 11 | issue = 5 | pages = 376–81 | date = 1991 | pmid = 1684039 | doi = 10.1002/j.1875-9114.1991.tb02648.x| url = }}</ref> |
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More serious side effects can include: |
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*] |
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*low blood pressure (]) |
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*skin reactions, e.g. ], hives, flaking of skin, worsening of ] |
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*sensation of ']' hands or feet |
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*irritated eyes, visual disturbances |
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*difficulty hearing |
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*difficulty speaking |
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*unsteadiness when walking |
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Serious side effects may require urgent medical attention. Some of these side effects are rare and others (not mentioned in the above list) can occur in some people. |
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Atenolol has been found to be safe in combination with the ] ] (MAOI) ] and actually improved ] and ] reactions with phenelzine.<ref name="Balon1998">{{cite book | vauthors = Gadde KM, Krishnan KR | chapter = Management of Side Effects of Monoamine Oxidase Inhibitors | veditors = Balon R | title=Practical Management of the Side Effects of Psychotropic Drugs | publisher=CRC Press | series=Medical Psychiatry Series | year=1998 | isbn=978-0-8247-4630-8 | chapter-url=https://books.google.com/books?id=VxKGwh5uQl8C&pg=PA71 | access-date=8 July 2024 | pages=67–83 (71) | quote = Interestingly, in one study, orthostatic hypotension was eliminated in a group of 61 patients treated for migraine headaches with phenelzine, when a beta-blocker, atenolol, was added (15). The authors have reported that hypertensive reactions were also less frequent when the two drugs were combined. We need further experience with this combination to determine whether addition of a beta-blocker is a safe and an effective strategy for alleviation of postural hypotension in depressed patients receiving an MAOI.}}</ref><ref name="OBrienOyebode2003">{{cite journal | vauthors = O'Brien P, Oyebode F | title=Psychotropic medication and the heart | journal=Advances in Psychiatric Treatment | volume=9 | issue=6 | date=2003 | issn=1355-5146 | doi=10.1192/apt.9.6.414 | pages=414–423 | quote = Postural hypotension is also a risk when antipsychotics are taken with β-blockers (probably because of pharmacokinetic interaction) or with diuretics (because of Na+ or volume depletion). The same hypotensive effects might be anticipated when tricyclic antidepressants or MAOIs are co-prescribed with peripheral antihypertensive agonists. One possible exception concerns phenelzine, whose hypotensive action was reversed on co-therapy with atenolol (Merikangas & Merikangas, 1995).}}</ref><ref name="MerikangasMerikangas1995">{{cite journal | vauthors = Merikangas KR, Merikangas JR | title = Combination monoamine oxidase inhibitor and beta-blocker treatment of migraine, with anxiety and depression | journal = Biol Psychiatry | volume = 38 | issue = 9 | pages = 603–610 | date = November 1995 | pmid = 8573662 | doi = 10.1016/0006-3223(95)00077-1 | url = | doi-access = free }}</ref> However, more research is still needed to assess whether addition of a beta blocker like atenolol to MAOI therapy is safe and effective for improving orthostatic hypotension with MAOIs.<ref name="Balon1998" /><ref name="MerikangasMerikangas1995" /> |
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===Asthma=== |
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Atenolol is classified as a β<sub>1</sub>-selective (or 'cardioselective') drug, one that exerts greater blocking activity on myocardial β<sub>1</sub>-receptors than on β<sub>2</sub> receptors in the lung. The β<sub>2</sub> receptors are responsible for keeping the bronchial system open. If these receptors are blocked, bronchospasm with serious lack of oxygen in the body can result. However, due to its cardioselective properties, the risk of bronchospastic reactions if using atenolol is reduced compared to nonselective drugs as ]. Nonetheless, this reaction may also be encountered with atenolol at high doses. Although traditionally B-blockers have been contraindicated when a person carries a diagnosis of asthma, recent studies have revealed that at moderate doses selective B blockers such as Atenolol are well tolerated. |
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==Pharmacology== |
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Provisional data suggests that antihypertensive therapy with atenolol provides weaker protective action against cardiovascular complications (e.g. myocardial infarction and ]) compared to other antihypertensive drugs. In some cases, ]s are superior. However, controlled studies are lacking.<ref name="pmid15530629">{{cite journal |author=Carlberg B, Samuelsson O, Lindholm LH |title=Atenolol in hypertension: is it a wise choice? |journal=Lancet |volume=364 |issue=9446 |pages=1684–9 |year=2004 |pmid=15530629 |doi=10.1016/S0140-6736(04)17355-8}}</ref> |
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===Pharmacodynamics=== |
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Unlike most other commonly-used β-blockers, atenolol is excreted almost exclusively by the ]s. This makes it attractive for use in individuals with end-stage ] disease. |
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Atenolol is a ]; that is, an ] of the ]s.<ref name="pmid33572109" /><ref name="TenorminLabel" /> It is specifically a ] antagonist of the ] with no ] (i.e., ] activity) or ].<ref name="pmid33572109" /><ref name="TenorminLabel" /> However, the preferential action of atenolol is not absolute, and at high doses, it can also block ]s.<ref name="TenorminLabel" /> |
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Beta-blocking effects of atenolol include reduction in ] and ] ] and ], reduction of ] and ] at rest and with exercise, inhibition of ] induced by ] (a non-selective β-adrenergic receptor ]), and reduction of ] orthostatic tachycardia.<ref name="TenorminLabel" /> |
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===Overdose=== |
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Symptoms of ] are due to excessive pharmacodynamic actions on β<sub>1</sub> and also β<sub>2</sub>-receptors. These include ], severe ] with ], acute ], ] and bronchospastic reactions. Treatment is largely symptomatic. Hospitalization and intensive monitoring is indicated. In early cases emesis can be induced. ] is useful to absorb the drug. ] will counteract bradycardia, ] helps with hypoglycemia, ] can be given against hypotension and the inhalation of a β<sub>2</sub>-mimetic as ] or ] will terminate bronchospasms. Blood or plasma atenolol concentrations may be measured to confirm a diagnosis of poisoning in hospitalized patients or to assist in a medicolegal death investigation. Plasma levels are usually less than 3 mg/L during therapeutic administration, but can range from 3–30 mg/L in overdose victims.<ref>DeLima LG, Kharasch ED, Butler S. Successful pharmacologic treatment of massive atenolol overdose: sequential hemodynamics and plasma atenolol concentrations. Anesthesiology 83:204-207, 1995.</ref><ref>R. Baselt, ''Disposition of Toxic Drugs and Chemicals in Man'', 8th edition, Biomedical Publications, Foster City, CA, 2008, pp. 116-117.</ref> |
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The beta-blocking effects of atenolol, as measured by reduction of exercise-related tachycardia, are apparent within 1{{nbsp}}hour and are maximal within 2 to 4{{nbsp}}hours following a single oral dose.<ref name="TenorminLabel" /> The general effects of atenolol, including beta-blocking and ] effects, last for at least 24{{nbsp}}hours following ] doses of 50 or 100{{nbsp}}mg.<ref name="TenorminLabel" /> With intravenous administration, maximal reduction in exercise-related tachycardia occurs within 5{{nbsp}}minutes and following a single 10{{nbsp}}mg dose has dissipated within 12{{nbsp}}hours.<ref name="TenorminLabel" /> The ] of atenolol is dose-related and is correlated with circulating levels of atenolol.<ref name="TenorminLabel" /> |
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==Pregnancy== |
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FDA pregnancy category D. This medication can cause harm to an unborn baby. Do not use atenolol if you are pregnant. Tell your doctor if you become pregnant during treatment. Use an effective form of birth control while you are using this medication. Atenolol can pass into breast milk and may harm a nursing baby. Do not use this medication without telling your doctor if you are breast-feeding a baby.<ref>{{cite web |url=http://www.drugsdb.eu/drug.php?d=Atenolol&m=State%20Of%20Florida%20Doh%20Central%20Pharmacy&id=b9f26cb9-7155-4c81-9b2e-7f1d72bddc46.xml |title=Atenolol, Prescription Marketed Drugs, www.drugsdb.eu}}</ref> |
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===Pharmacokinetics=== |
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==Pharmacokinetic data== |
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====Absorption==== |
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*t<sub>cmax</sub> = 2 to 4 hours after oral dosing (time elapsed before maximal concentration in the ] is reached) |
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The ] ] of atenolol is approximately 50 to 60%.<ref name="WadworthMurdochBrogden1991" /><ref name="HeelBrogdenSpeight1979" /> The ] of atenolol with oral administration is rapid and consistent but is incomplete.<ref name="TenorminLabel" /> About 50% of an oral dose of atenolol is absorbed from the ]s, with the rest ] in ].<ref name="TenorminLabel" /> ]s of atenolol occur 2 to 4{{nbsp}}hours following an oral dose, whereas peak concentrations occur within 5{{nbsp}}minutes with ].<ref name="TenorminLabel" /> The ] profile of atenolol results in it having relatively consistent plasma drug levels with about 4-fold variation between individuals.<ref name="TenorminLabel" /> |
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*The mean elimination ] is 6 hours. However, the action of the usual oral dose of 25 to 100 mg lasts over a period of 24 hours. |
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*Atenolol is a ] drug. The concentration found in brain tissue is approximately 15% of the plasma concentration only. The drug crosses the ] barrier freely. In the milk of ] mothers, approximately 3 times the plasma concentrations are measured. |
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*Atenolol is almost exclusively eliminated ] and is well removable by ]. A compromised ] function does not lead to higher peak-activity and/or a longer halflife with possible accumulation. |
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====Distribution==== |
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==References== |
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The ] of atenolol is 6 to 16%.<ref name="TenorminLabel" /> |
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{{Reflist|30em}} |
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Atenolol is classified as a beta blocker with low ] and hence lower potential for crossing the ] and entering the brain.<ref name="pmid33572109">{{cite journal | vauthors = Cojocariu SA, Maștaleru A, Sascău RA, Stătescu C, Mitu F, Leon-Constantin MM | title = Neuropsychiatric Consequences of Lipophilic Beta-Blockers | journal = Medicina (Kaunas) | volume = 57 | issue = 2 | date = February 2021 | page = 155 | pmid = 33572109 | pmc = 7914867 | doi = 10.3390/medicina57020155 | url = | doi-access = free }}</ref> This in turn may result in fewer effects in the ] as well as a lower risk of ] side effects.<ref name="pmid33572109" /> Only small amounts of atenolol are said to enter the brain.<ref name="WadworthMurdochBrogden1991" /><ref name="HeelBrogdenSpeight1979" /> The brain-to-blood ratio of atenolol was 0.2 : 1 in one study, whereas the ratio for propranolol was 33 : 1 in the same study.<ref name="HeelBrogdenSpeight1979" /> |
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==External links== |
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* U.S. National Library of Medicine: Drug Information Portal |
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====Metabolism==== |
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{{Antihypertensives}} |
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Atenolol undergoes minimal or negligible ] by the ].<ref name="TenorminLabel" /><ref name="BroddeKroemer2003" /> It has been estimated that about 5% of atenolol is metabolized.<ref name="KirchGörg1982">{{cite journal | vauthors = Kirch W, Görg KG | title = Clinical pharmacokinetics of atenolol--a review | journal = Eur J Drug Metab Pharmacokinet | volume = 7 | issue = 2 | pages = 81–91 | date = 1982 | pmid = 6749509 | doi = 10.1007/BF03188723 | url = }}</ref> This is in contrast to other beta blockers like ] and ], but is similar to ].<ref name="TenorminLabel" /> In accordance with its lack of hepatic metabolism, the pharmacokinetics of atenolol are not altered in ], unlike the case of propranolol.<ref name="BroddeKroemer2003" /> Two ]s of atenolol have been identified: hydroxyatenolol and atenolol glucuronide.<ref name="WadworthMurdochBrogden1991" /> It has been said that it is unknown if these metabolites are active.<ref name="WadworthMurdochBrogden1991" /> However, another source stated that hydroxyatenolol has one-tenth the beta-blocking activity of atenolol.<ref name="HeelBrogdenSpeight1979" /> |
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====Elimination==== |
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Instead of by hepatic metabolism, atenolol is ] from the blood mainly via ] ].<ref name="TenorminLabel" /> Atenolol is excreted about 40 to 50% in ] and 50% in ] with oral administration.<ref name="HeelBrogdenSpeight1979">{{cite journal | vauthors = Heel RC, Brogden RN, Speight TM, Avery GS | title = Atenolol: a review of its pharmacological properties and therapeutic efficacy in angina pectoris and hypertension | journal = Drugs | volume = 17 | issue = 6 | pages = 425–460 | date = June 1979 | pmid = 38096 | doi = 10.2165/00003495-197917060-00001 | url = }}</ref><ref name="TenorminLabel" /> Conversely, it is excreted 85 to 100% in urine unchanged and 10% in feces with intravenous administration.<ref name="HeelBrogdenSpeight1979" /><ref name="TenorminLabel" /> Only very small amounts of hydroxyatenolol and atenolol glucuronide are found in urine with atenolol.<ref name="HeelBrogdenSpeight1979" /> |
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The ] of atenolol is about 6 to 7{{nbsp}}hours.<ref name="TenorminLabel" /> The half-life of atenolol does not change with continuous administration.<ref name="TenorminLabel" /> With intravenous administration, atenolol levels rapidly decline (5- to 10-fold) during the first 7{{nbsp}}hours and thereafter decline at a rate similar to that with oral administration.<ref name="TenorminLabel" /> |
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The elimination of atenolol is slowed in ], with the elimination rate being closely related to the ] (GFR) and with significant accumulation occurring when the ] ] rate is under 35{{nbsp}}mL/min/1.73{{nbsp}}m<sup>2</sup>.<ref name="TenorminLabel" /> At a GFR of less than 10{{nbsp}}mL/min, the half-life of atenolol increases up to 36{{nbsp}}hours.<ref name="KirchGörg1982" /> |
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==Chemistry== |
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Atenolol is a ] ].<ref name="PubChem" /> It is specifically ] with an α-keto ] and a 4- substitution on the ].<ref name="PubChem" /> |
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The experimental ] of atenolol is 0.16 and its predicted log P ranges from −0.03 to 0.57.<ref name="PubChem">{{cite web | title=Atenolol | website=PubChem | url=https://pubchem.ncbi.nlm.nih.gov/compound/2249 | access-date=1 August 2024}}</ref><ref name="DrugBank">{{cite web | title=Atenolol: Uses, Interactions, Mechanism of Action | website=DrugBank Online | date=13 August 2004 | url=https://go.drugbank.com/drugs/DB00335 | access-date=1 August 2024}}</ref><ref name="ChemSpider">{{cite web | title=DL-Atenolol | website=ChemSpider | date=21 July 2022 | url=https://www.chemspider.com/Chemical-Structure.2162.html | access-date=1 August 2024}}</ref> |
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Atenolol is closely ] to metoprolol and certain other beta blockers. It is also structurally related to the ] ]s ] (adrenaline) and ] (noradrenaline). |
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==Society and culture== |
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===Changing medical practices=== |
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Atenolol has been given as an example of how slow healthcare providers are to change their prescribing practices in the face of ] that indicates that a drug is not as effective as others in treating some conditions.<ref name=":0">{{cite news|url=https://www.theatlantic.com/health/archive/2017/02/when-evidence-says-no-but-doctors-say-yes/517368/|title=When Evidence Says No, But Doctors Say Yes|vauthors=Epstein D|date=22 July 2017|newspaper=]|access-date=8 May 2018|archive-date=9 May 2018|archive-url=https://web.archive.org/web/20180509150759/https://www.theatlantic.com/health/archive/2017/02/when-evidence-says-no-but-doctors-say-yes/517368/|url-status=live}}</ref> In 2012, 33.8 million prescriptions were written to American patients for this drug.<ref name=":0"/> In 2014, it was in the top (most common) 1% of drugs prescribed to Medicare patients.<ref name=":0"/> Although the number of prescriptions has been declining steadily since limited evidence articles contesting its efficacy was published, it has been estimated that it would take 20 years for doctors to stop prescribing it for hypertension.<ref name=":0"/> Despite its diminished efficacy when compared to newer ]s, atenolol and other ]s are still a relevant clinical choice for treating some conditions, since ]s are a diverse group of medicines with different properties that still requires further research.<ref name="Cochrane2017" /> As consequence, reasons for the popularity of beta blockers cannot be fully attributed to a slow healthcare system – ] factor, such as treatment cost and duration, also affect adherence and popularity of therapy.<ref>{{cite journal | vauthors = Choi HY, Oh IJ, Lee JA, Lim J, Kim YS, Jeon TH, Cheong YS, Kim DH, Kim MC, Lee SY | title = Factors Affecting Adherence to Antihypertensive Medication | journal = Korean Journal of Family Medicine | volume = 39 | issue = 6 | pages = 325–332 | date = November 2018 | pmid = 30384549 | pmc = 6250947 | doi = 10.4082/kjfm.17.0041 }}</ref> |
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== References == |
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{{Reflist}} |
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{{Beta blockers}} |
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{{Adrenergics}} |
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{{Adrenergics}} |
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{{AstraZeneca}} |
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{{AstraZeneca}} |
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{{Portal bar | Medicine}} |
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