VASODILATION TO ACETYLCHOLINE IN PRIMARY AND SECONDARY FORMS OF HUMANHYPERTENSION

Citation
S. Taddei et al., VASODILATION TO ACETYLCHOLINE IN PRIMARY AND SECONDARY FORMS OF HUMANHYPERTENSION, Hypertension, 21(6), 1993, pp. 929-933
Citations number
25
Categorie Soggetti
Cardiac & Cardiovascular System
Journal title
ISSN journal
0194911X
Volume
21
Issue
6
Year of publication
1993
Part
2
Pages
929 - 933
Database
ISI
SICI code
0194-911X(1993)21:6<929:VTAIPA>2.0.ZU;2-R
Abstract
Endothelium-dependent vasodilatation to acetylcholine is reduced in th e forearm of essential hypertensive patients. To investigate whether e ndothelium-dependent vasodilatation is reduced also in secondary hyper tension, we evaluated the effects of an intrabrachial infusion of acet ylcholine 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 co ntrol subjects (n=12). To further evaluate the role of a cyclooxygenas e-dependent endothelium-derived vasoconstrictor substance, we repeated the infusion of acetylcholine in the presence of indomethacin. The ef fect 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 n ormotensive subjects. In contrast, the vasodilatation induced by sodiu m nitroprusside was similar in all groups of patients and control subj ects. In the presence of indomethacin, the vasodilator effect of acety lcholine was increased in essential hypertensive patients but not in n ormotensive or in secondary hypertensive individuals. These data demon strate an impairment of endothelium-dependent vasodilation in renovasc ular and primary aldosteronism hypertensive patients and indicate that a cyclooxygenase-dependent vasoconstrictor mechanism participates in the blunting of endothelium-dependent vasodilation in essential hypert ensive patients.