Role of alpha-adrenergic blockade in the cardiovascular actions of ketanserin: studies in patients with essential hypertension, autonomic insufficiency, and Raynaud's phenomenon.
It remains to be established whether ketanserin's antihypertensive effect is caused by S2-serotonergic blockade, by alpha 1-adrenergic blockade, or by a combination of both. Ketanserin, 10 mg i.v. or 40 mg t.i.d. orally, blocked the serotonin-induced contractions of hand veins in patients with essential hypertension. Intravenous ketanserin had no effect on the venoconstrictor action of noradrenaline. The increase in digital blood flow after i.v. ketanserin, as measured by the change in digital skin temperature in patients with Raynaud's phenomenon, was not blocked by phentolamine or pretreatment with prazosin. Intravenous ketanserin also lowered arterial pressure in patients with autonomic insufficiency who were unresponsive to phentolamine. These observations suggest that alpha-adrenergic blockade is not the sole mechanism of ketanserin's cardiovascular actions in humans.
D000317:Adrenergic alpha-Antagonists; D000328:Adult; D000368:Aged; D001342:Autonomic Nervous System Diseases / Q000188:drug therapy* / Q000503:physiopathology; D001794:Blood Pressure / Q000187:drug effects; D006801:Humans; D006973:Hypertension / Q000188:drug therapy* / Q000503:physiopathology; D007223:Infant; D007650:Ketanserin / Q000494:pharmacology*; D008297:Male; D008875:Middle Aged; D011928:Raynaud Disease / Q000188:drug therapy* / Q000503:physiopathology; D012039:Regional Blood Flow / Q000187:drug effects; D014661:Vasoconstriction / Q000187:drug effects
D000317:Adrenergic alpha-Antagonists; D007650:Ketanserin