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beta-adrenergic blocker

   Also found in: Medical, Encyclopedia, Wikipedia 0.01 sec.
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Noun1.beta-adrenergic blocker - any of various drugs used in treating hypertension or arrhythmia; decreases force and rate of heart contractions by blocking beta-adrenergic receptors of the autonomic nervous system
acebutolol, Sectral - an oral beta blocker (trade name Sectral) used in treating hypertension
atenolol, Tenormin - an oral beta blocker (trade name Tenormin) used in treating hypertension and angina; has adverse side effects (depression and exacerbation of congestive heart failure etc.)
blocking agent, blocker - a class of drugs that inhibit (block) some biological process
carvedilol - beta blocker that can reduce the progression of heart failure in individuals whose disease is not advanced
Brevibloc, esmolol - intravenous beta blocker (trade name Brevibloc) that acts for only a short time; used primarily for cardiac arrhythmias
Lopressor, metoprolol - beta blocker (trade name Lopressor) used in treating hypertension and angina and arrhythmia and acute myocardial infarction; has adverse side effects (depression and exacerbation of congestive heart failure etc.)
Corgard, nadolol - a beta-adrenergic blocking agent (trade name Corgard) that is used to treat hypertension and angina
pindolol, Visken - an oral beta blocker (trade name Visken) used in treating hypertension
Inderal, propanolol - the first beta blocker (trade name Inderal) used in treating hypertension and angina pectoris and essential tremor
Blocadren, timolol - a beta blocker (trade name Blocadren) administered after heart attacks


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This presentation concluded that CK-1122534 increases the fractional shortening in ventricular myocytes (a measure of cardiac contractility) in a dose-dependent manner, does not increase the calcium transient, does not inhibit phosphodiesterase (PDE) activity and is active in the presence of a beta-adrenergic blocker.
Furthermore, Cytokinetics presented results that demonstrated that CK-1122534 does not increase the calcium transient and does not inhibit phosphodiesterase activity and that the attendant increase in fractional shortening is not attenuated by the addition of a beta-adrenergic blocker, altogether providing evidence that CK-1122534 increases myocyte contractility by directly activating cardiac myosin.
 
 
 
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