| Revision as of 13:01, 13 April 2006 editSilverback (talk | contribs)6,113 edits →Operation: wordsmithing← Previous edit | Revision as of 01:32, 14 April 2006 edit undoCHurst5841 (talk | contribs)13 edits →OperationNext edit → | ||
| Line 4: | Line 4: | ||
| == Operation == | == Operation == | ||
| Beta blockers block the action of ] and ] on the β-]s in the body |
Beta blockers block the action of catecholamines (] and ]) on the β-]s in the body. It is important to note that both hormones and neurotransmitters stimulate the ] through action on these receptors. | ||
| There are three types of beta receptors: β<sub>1</sub>-receptors located mainly in the heart, and β<sub>2</sub>-receptors located |
There are three types of beta receptors: β<sub>1</sub>-receptors located mainly in the heart, kidney, and adipose tissue and β<sub>2</sub>-receptors located in the lung, GI tract, liver, pancreas, and skeletal muscle. β<sub>3</sub>-receptors are less well characterized, but function in fat metabolism and are thus thought to have a role in obesity. | ||
| Stimulation of β<sub>1</sub>-receptors by epinephrine induces a positive chronotropic and inotropic effect on the heart and increases cardiac conduction velocity and automaticity. Drugs that block these receptors therefore have the reverse effect: they exert a negative chronotropic and inotropic effect and decrease cardiac conduction veolocity and automaticity. Furthermore, β<sub>1</sub> blockade also inhibits kidney renin secretion and lipolysis. They are routinely prescribed in patients with ], ], and cardiac arrythmias. | |||
| Many beta blockers affect both type 1 and type 2 receptors and are classified as <i>noncardioselective</i> beta blockers (e.g. ], ], etc.). <i>Cardioselective</i> beta blockers (e.g. acebutolol, atenolol, etc.) primarily affect β<sub>1</sub>-receptors. Beta blocker therapy is contraindicated in asthmatics and individuals prone to exercise induced bronchoconstriction. If beta blocker therapy is indicated in either case, preference must be given to cardioselective drugs to avoid bloking the β<sub>2</sub> mediated relaxation of the bronchii. | |||
| ⚫ | Drugs that block β<sub>2</sub> receptors generally have a calming effect and are prescribed for ], ], ] |
||
| ⚫ | Drugs that block β<sub>2</sub> receptors generally have a calming effect and are prescribed for ], ], ], ], etc. | ||
| Many beta blockers affect both type 1 and type 2 receptors; these are termed ''non-selective'' blockers. ] and ] are examples. Selective beta blockers primarily affect β<sub>1</sub>-receptors. Non-selective beta blockers should generally not be used in patients with ] or any reactive airway disease. Doing so can precipitate ] by blocking the β<sub>2</sub> mediated relaxation of the bronchiole muscles. | |||
| Selective beta blockers generally only block the type 1 receptor. They gradually become less selective at higher doses. Examples of selective beta<sub>1</sub> blockers in common use include ] and ]. | |||
| Since they lower heart rate, beta blockers have been used by some ] ] to provide more aiming time between ]s. Some ] use beta blockers to avoid ] and tremor during ]s and ]s. Beta blockers decrease nocturnal ] release, perhaps explaining the impotence side effect through suppression of morning erections. | Since they lower heart rate, beta blockers have been used by some ] ] to provide more aiming time between ]s. Some ] use beta blockers to avoid ] and tremor during ]s and ]s. Beta blockers decrease nocturnal ] release, perhaps explaining the impotence side effect through suppression of morning erections. | ||
Revision as of 01:32, 14 April 2006
You must add a |reason= parameter to this Cleanup template – replace it with {{Cleanup|February 2006|reason=<Fill reason here>}}, or remove the Cleanup template.
Beta blockers or beta-adrenergic blocking agents are a class of drugs used to treat a variety of cardiovascular conditions and some other diseases.
Operation
Beta blockers block the action of catecholamines (epinephrine and norepinephrine) on the β-adrenergic receptors in the body. It is important to note that both hormones and neurotransmitters stimulate the sympathetic nervous system through action on these receptors.
There are three types of beta receptors: β1-receptors located mainly in the heart, kidney, and adipose tissue and β2-receptors located in the lung, GI tract, liver, pancreas, and skeletal muscle. β3-receptors are less well characterized, but function in fat metabolism and are thus thought to have a role in obesity.
Stimulation of β1-receptors by epinephrine induces a positive chronotropic and inotropic effect on the heart and increases cardiac conduction velocity and automaticity. Drugs that block these receptors therefore have the reverse effect: they exert a negative chronotropic and inotropic effect and decrease cardiac conduction veolocity and automaticity. Furthermore, β1 blockade also inhibits kidney renin secretion and lipolysis. They are routinely prescribed in patients with ischemic heart disease, hypertension, and cardiac arrythmias.
Many beta blockers affect both type 1 and type 2 receptors and are classified as noncardioselective beta blockers (e.g. propranolol, nadolol, etc.). Cardioselective beta blockers (e.g. acebutolol, atenolol, etc.) primarily affect β1-receptors. Beta blocker therapy is contraindicated in asthmatics and individuals prone to exercise induced bronchoconstriction. If beta blocker therapy is indicated in either case, preference must be given to cardioselective drugs to avoid bloking the β2 mediated relaxation of the bronchii.
Drugs that block β2 receptors generally have a calming effect and are prescribed for anxiety, migraine, esophageal varices, alcohol withdrawal syndrome, etc.
Since they lower heart rate, beta blockers have been used by some Olympic marksmen to provide more aiming time between heart beats. Some musicians use beta blockers to avoid stage fright and tremor during auditions and performances. Beta blockers decrease nocturnal melatonin release, perhaps explaining the impotence side effect through suppression of morning erections.
- Stoschitzky K, Sakotnik A, Lercher P, Zweiker R, Maier R, Liebmann P, Lindner W. Influence of beta-blockers on melatonin release. Eur J Clin Pharmacol. 1999 Apr;55(2):111-5. PMID 10335905
Beta Blockers at a Glance
By receptor type:
- Beta 1 selective (Cardio selective): Atenolol, Acebutolol, Betaxolol, Bisoprolol, Esmolol, Metoprolol, Nebivolol.
- Preferable in points with bronchospastic disease, diabetes, peripheral vascular ds. e.g. Raynaud’s phenomenon (bronchoconstriction, inhibition of glycogenolysis, vasoconstriction are due to β2 blockade)
- Beta 2 selective—Butoxamine
- Additional a1 antagonistic activity: Bucindolol, Carvedilol, Labetolol, Medroxolol
- Potentially advantageous in points with hypertension, occlusive peripheral artery ds. (promote vasodilatation)
- Partial agonist (intrinsic sympathomimetic) activity: Acebutolol, Bopindolol, Carteolol, Celiprolol*, Labetolol, Oxiprenolol, Penbutolol, Pindolol (Beta 1 selective antagonist with β2-agonist activity; also has non-adrenergic receptor-mediated vasodilating property.)
- Potentially advantageous in points with hypertension, occlusive peripheral artery ds. (Promote vasodilatation)
- Less likely to cause bradycardia, bronchoconstriction, lipid abnormalities.
- Local anaesthetic action (membrane stabilizing property/ Na channel blockade): Acebutolol, Propranolol, Propafenone; slight activity: Betaxolol, Labetolol, Metoprolol, Pindolol
By lipid solubility:
- High: Propranolol, Penbutolol
- Readily cross BBB—central effects, large volume of distribution
- Low: Atenolol, Esmolol, Nadolol
- Don’t cross BBB—no central effects
By half-life:
- Long: Betaxolol, Nadolol (14–22 hours)
- OD dosing.
- Shortest: Esmolol (8–10 minute)
- Hydrolyzed by esterases in erythrocytes)
- Given as intravenous infusion in urgent settings.
- Intermediate: between 3 and 12 hours
By oral bioavailability:
- High: Betaxolol, Pindolol, Penbutolol, and Sotalol
- Low: Carvedilol, Esmolol, Labetolol, Nadolol, Propranolol
Miscellaneous:
- No effect on plasma rennin activity: Pindolol
- Anti-oxidant activity: Carvedilol
- Antiarrythmic action (independent of β-blocking action): Sotalol
Uses
- Hypertension
- Prophylaxis of angina
- Prophylaxis of MI—Metoprolol, Propranolol, Timolol
- Mild-moderate CHF (Contraindicated in compensated heart failure) – Bisoprolol, Bucindolol, Carvedilol, Metoprolol
- Hypertrophic obstructive cardiomyopathy – esp. Propranolol
- Pheochromocytoma (a blocker given before β-blocker)
- Acute dissecting aortic aneurysm
- Marfan’s syndrome (Chr. Tt. with Propran. slows progression of aortic dilatation and its complications)
- Hyperthyroidism
- Prophylaxis of Migraine — Metoprolol, Propranolol, Timolol
- Somatic manifestations of anxiety (e.g. tremors) — Propranolol
- Glaucoma (↓ aqueous production) — Betaxolol, Carteolol, Levobunolol, Metipranolol, Timolol
- Prevention of vericial bleeding in portal hypertension -Propranolol, Nadolol
External links
- Musicians using beta blockers
- Better Playing Through Chemistry by Blair Tindall, New York Times, October 17, 2004. (Discussing the use of beta-blockers among professional musicians.)
| Beta blockers (C07) | |
|---|---|
| β, non-selective | |
| β1-selective | |
| β2-selective | |
| α1- + β-selective | |
| |