2/29/2024 0 Comments Er capsIn angina pectoris, propranolol generally reduces the oxygen requirement of the heart at any given level of effort by blocking the catecholamine-induced increases in the heart rate, systolic blood pressure, and the velocity and extent of myocardial contraction. Effects of propranolol on plasma volume appear to be minor and somewhat variable. Although total peripheral resistance may increase initially, it readjusts to or below the pretreatment level with chronic use of propranolol. Among the factors that may be involved in contributing to the antihypertensive action include: (1) decreased cardiac output, (2) inhibition of renin release by the kidneys, and (3) diminution of tonic sympathetic nerve outflow from vasomotor centers in the brain. ![]() The mechanism of the antihypertensive effect of propranolol has not been established. In most clinical settings, however, such as hypertension or angina where there is little correlation between plasma levels and clinical effect, propranolol hydrochloride extended-release capsules have been therapeutically equivalent to the same mg dose of conventional propranolol hydrochloride as assessed by 24-hour effects on blood pressure and on 24-hour exercise responses of heart rate, systolic pressure, and rate pressure product. When changing to propranolol hydrochloride extended-release capsules from conventional propranolol, a possible need for retitration upwards should be considered, especially to maintain effectiveness at the end of the dosing interval. Propranolol hydrochloride extended-release capsules should not be considered a simple mg-for-mg substitute for conventional propranolol and the blood levels achieved do not match (are lower than) those of two to four times daily dosing with the same dose (see DOSAGE AND ADMINISTRATION). The significance of the membrane action in the treatment of arrhythmias is uncertain. At dosages greater than required for beta blockade, propranolol also exerts a quinidine-like or anesthetic-like membrane action, which affects the cardiac action potential. When access to beta-receptor sites is blocked by propranolol, the chronotropic, inotropic, and vasodilator responses to beta-adrenergic stimulation are decreased proportionately. It specifically competes with beta-adrenergic receptor-stimulating agents for available receptor sites. Propranolol is a nonselective, beta-adrenergic receptor-blocking agent possessing no other autonomic nervous system activity. These capsules comply with USP Dissolution Test 1. Propranolol hydrochloride extended-release 120 mg capsules contain FD&C Blue No. In addition, propranolol hydrochloride extended-release 80 mg, and 160 mg capsules contain D&C Red No. The inactive ingredients contained in propranolol hydrochloride extended-release capsules are: cellulose, ethylcellulose, gelatin capsules, hypromellose, and titanium dioxide. Propranolol hydrochloride extended-release capsules are available as 60 mg, 80 mg, 120 mg, and 160 mg capsules for oral administration. Propranolol hydrochloride extended-release capsules are formulated to provide a sustained release of propranolol hydrochloride. Propranolol hydrochloride is a stable, white, crystalline solid which is readily soluble in water and ethanol. ![]() Its molecular and structural formulae are: ![]() Propranolol hydrochloride is a synthetic beta-adrenergic receptor-blocking agent chemically described as 2-Propanol, 1-3-(1-naphthalenyloxy)-, hydrochloride,(±).
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