Vasodilation to acetylcholine in primary and secondary forms of human hypertension.

Abstract

Endothelium-dependent vasodilatation to acetylcholine is reduced in the forearm of essential hypertensive patients. To investigate whether endothelium-dependent vasodilatation is reduced also in secondary hypertension, we evaluated the effects of an intrabrachial infusion of acetylcholine on forearm blood flow (strain-gauge venous plethysmography) in essential hypertensive (n = 12), primary aldosteronism hypertensive (n = 8), and renovascular hypertensive (n = 8) patients and normotensive control subjects (n = 12). To further evaluate the role of a cyclooxygenase-dependent endothelium-derived vasoconstrictor substance, we repeated the infusion of acetylcholine in the presence of indomethacin. The effect of the direct vasodilator sodium nitroprusside was also examined. The vasodilatation to acetylcholine was reduced in essential, primary aldosteronism, and renovascular hypertensive patients compared with normotensive subjects. In contrast, the vasodilatation induced by sodium nitroprusside was similar in all groups of patients and control subjects. In the presence of indomethacin, the vasodilator effect of acetylcholine was increased in essential hypertensive patients but not in normotensive or in secondary hypertensive individuals. These data demonstrate an impairment of endothelium-dependent vasodilation in renovascular and primary aldosteronism hypertensive patients and indicate that a cyclooxygenase-dependent vasoconstrictor mechanism participates in the blunting of endothelium-dependent vasodilation in essential hypertensive patients.