![]() This contrasts with the effect of nonselective (beta 1 plus beta 2) beta-blockers, which completely reverse the vasodilating effects of epinephrine. Relative beta 1 selectivity is demonstrated by the following: (1) In healthy subjects, metoprolol is unable to reverse the beta 2-mediated vasodilating effects of epinephrine. The precise mechanism of action of metoprolol in patients with suspected or definite myocardial infarction is not known. Angina Pectorisīy blocking catecholamine-induced increases in heart rate, in velocity and extent of myocardial contraction, and in blood pressure, metoprolol reduces the oxygen requirements of the heart at any given level of effort, thus making it useful in the long-term management of angina pectoris. ![]() However, several possible mechanisms have been proposed: (1) competitive antagonism of catecholamines at peripheral (especially cardiac) adrenergic neuron sites, leading to decreased cardiac output (2) a central effect leading to reduced sympathetic outflow to the periphery and (3) suppression of renin activity. The mechanism of the antihypertensive effects of beta-blocking agents has not been fully elucidated. This preferential effect is not absolute, however, and at higher plasma concentrations, metoprolol also inhibits beta 2 adrenoreceptors, chiefly located in the bronchial and vascular musculature.Ĭlinical pharmacology studies have demonstrated the beta-blocking activity of metoprolol, as shown by (1) reduction in heart rate and cardiac output at rest and upon exercise, (2) reduction of systolic blood pressure upon exercise, (3) inhibition of isoproterenol-induced tachycardia, and (4) reduction of reflex orthostatic tachycardia. Metoprolol is a beta 1-selective (cardioselective) adrenergic receptor blocker.
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