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Am J Physiol Heart Circ Physiol 278: H168-H174, 2000;
0363-6135/00 $5.00
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Vol. 278, Issue 1, H168-H174, January 2000

Impaired endothelium-mediated vasodilation is not the principal cause of vasoconstriction in heart failure

Carlos E. Negrao1, Michele A. Hamilton2, Gregg C. Fonarow2, Antoine Hage2, Jaime D. Moriguchi2, and Holly R. Middlekauff2

2 Division of Cardiology, Department of Medicine, University of California School of Medicine, Los Angeles, California 90095; and 1 Laboratory of Cardiovascular Physiology in Exercise, Heart Institute, University of Sao Paulo, School of Medicine, Sao Paulo, 05403-000, Brazil

The extent to which abnormal endothelium-dependent vasodilator mechanisms contribute to abnormal resting vasoconstriction and blunted reflex vasodilation seen in heart failure is unknown. The purpose of this study was to test the hypothesis that the resting and reflex abnormalities in vascular tone that characterize heart failure are mediated by abnormal endothelium-mediated mechanisms. Thirteen advanced heart-failure patients (New York Heart Association III-IV) and 13 age-matched normal controls were studied. Saline, acetylcholine (20 µg/min), or L-arginine (10 mg/min) was infused into the brachial artery, and forearm blood flow was measured by venous plethysmography at rest and during mental stress. At rest, acetylcholine decreased forearm vascular resistance in normal subjects, but this response was blunted in heart failure. During mental stress with intra-arterial acetylcholine or L-arginine, the decrease in forearm vascular resistance was not greater than during saline control in heart failure [saline control vs. acetylcholine (7 ± 3 vs. 6 ± 3, P = NS) or vs. L-arginine (9 ± 2 units, P = NS)]. The increase in forearm blood flow was not greater than during saline control in heart failure [saline control vs. acetylcholine (1.2 ± 0.3 vs. 1.3 ± 0.3, P = NS), or vs. L-arginine (1.2 ± 0.2 ml · min-1 · 100 ml-1, P = NS)]. Furthermore, during mental stress with nitroprusside, the decrease in forearm vascular resistance was not greater than during saline control [saline control vs. nitroprusside (7 ± 3 vs. 5 ± 4 ml · min-1 · 100 g-1, P = NS)], and the increase in forearm blood flow was not greater than during saline control [saline control vs. nitroprusside (1.2 ± 0.3 vs. 1.3 ± 0.5 ml · min-1 · 100 g-1, P = NS)]. Because the endothelial-independent agent nitroprusside was unable to restore resting and reflex vasodilation to normal in heart failure, we conclude that impaired endothelium-mediated vasodilation with acetylholine-nitric oxide cannot be the principal cause of the attenuated resting- or reflex-mediated vasodilation in heart failure.

nitric oxide; mental stress


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