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Mechanism of action of ketanserin in hypertension and vasospastic disease.

It remains to be established whether ketanserin's antihypertensive effect is caused by blockade of serotonergic type 2 receptors (S2), by blockade of alpha 1-adrenoceptors or by combined effect on both receptors. We therefore performed several clinical studies. Ketanserin, 10 mg i.v., lowered blood pressure in 6 patients with essential hypertension and blocked, at the same time, the contraction of hand veins to exogenous serotonin. In contrast, ketanserin had no effect on the venoconstrictor action of noradrenaline. Ketanserin also did not alter the pressor effect of bolus injections of the alpha 1-agonist phenylephrine. Furthermore, ketanserin had a distinct hypotensive effect in 4 normotensive patients with autonomic insufficiency who were unresponsive to alpha 1-adrenoceptor blockade. Moreover, the ketanserin-induced marked increase in digital blood flow in 7 patients with Raynaud's phenomenon was not blocked by pretreatment with high doses of the alpha 1-adrenoceptor blockade. However, in patients with essential hypertension, the antihypertensive effect of ketanserin was blunted by pretreatment with prazosin. This may be related to S2 blockade of the alleged amplifying effect of serotonin on alpha 1-adrenoceptor mediated vasoconstriction but the data do not exclude concomitant alpha-blockade by ketanserin. We conclude that the mechanism of ketanserin's antihypertensive effect requires further clarification; nevertheless the data cited above do not support the view that ketanserin is nothing more than another alpha-blocker.