Adverse effects of antihypertensive agents

a-Blockers and fj-blockers are being used extensively for the treatment of hypertension. Endogenous or drug­induced increases in circulating levels of adrenaline and/ or noradrenaline could modify the antihypertensive effect of these agents in some patients. Thus, during long term treatment with propranolol, about 11 % of patients with essentia1 bypertension showed a still further increase in their BP. Propranolol is known to stimulate catecholamine secretion through a direct effect on the adrenal medulla. High levels of catecholamines could stimulate a-adrenergic receptors with resultant increases in BP, because the vasodilator action of adrenaline on peripheral i3-receptors, which would normally attenuate the vasoconstrictor a-receptor effect, is blocked during treatment with a {3-blocker such as propranolol. Prazosin and phenoxYbenzamine (antagonists of the postsynaptic ai-receptors) lower B~. but both drujl.s also induce noradrenaline secretion. In the presence of a­receptor blockade, it is possible that sensitivity of {J­receptors to noradrenaline is increased. The resulting vasodilatation could enhance the antihypertensive action of these drugs. Less frequently, a pressor response has been noted with acute administration of oral c1onidine, as well as concurrent administration of a-and ,B-receptor blockers (e.g. c10nidine and propranolol). Catecholamines are considered to be responsible for the adverse effects. Catecholamine-mediated pressor responses are probably less likely to occur with cardioselective ,B-adrenergic sympatholytic agents. Drayer. J.I.M . et a" : American Heart Journal 104: 660 (Sep 1982)

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