Impaired acetylcholine-mediated vasodilation in patients with congestive heart failure. Role of endothelium-derived vasodilating and vasoconstricting factors.

• DOI: 10.1161/01.cir.88.1.55
• Publication Date: 2012-06-12T00:01:09Z
• Authors: S D Katz; M Schwarz; J Yuen; T H LeJemtel
• Keywords: Vasodilator agents; Endothelial Dysfunction

BACKGROUND The vasodilatory response to intra-arterial administration of acetylcholine is reduced in patients with congestive heart failure compared that normal subjects. may be related decreased endothelial release nitric oxide, interaction peripheral alpha-adrenergic transmission, or production cyclooxygenase-dependent vasoconstricting substances. extent which each these mechanisms contributes the not known. METHODS AND RESULTS Thirty-one (New York Heart Association functional class II-III) and five age-matched subjects were studied. Regional vascular responses forearm infusions acetylcholine, an endothelium-dependent vasodilator (10(-7) 10(-5) mol/L) nitroglycerin, endothelium-independent (10(-6) brachial artery determined venous occlusion plethysmography before after regional blockade phentolamine (25 micrograms/min) systemic cyclooxygenase oral indomethacin (50 mg). Administration significantly increased resting baseline blood flow 11 (2.9 +/- 0.4 5.4 0.8 mL.min-1.100 mL-1) (4.6 0.3 11.3 2.1 mL-1). Before phentolamine, 10(-7), 10(-6), mol/L 4.0 1.0, 6.0 1.7, 16.1 mL-1, respectively, 14.7 6.2, 20.2 4.7, 38.7 7.9 After nitroglycerin did change either alter 15 (2.7 2.7 infusion by average 39% but In failure, less than those both indomethacin. CONCLUSIONS probably results from several coexistent abnormalities function, including abnormal factor, impaired smooth muscle responsiveness cyclic GMP-mediated vasodilation.