Endothelial function in congestive heart failure

Helmut Drexler, Daniel Hayoz, Thomas Münzel, Hanjörg Just, Robert Zelis, Hans R. Brunner

Research output: Contribution to journalArticlepeer-review

15 Scopus citations


There is evidence that the endothelium plays an important role in the control of human vascular tone by releasing endothelium-derived nitric oxide and, therefore, a defective endothelial function could be involved in the increased peripheral vasoconstriction of patients with chronic congestive heart failure. To investigate endothelial function in humans in vivo, agents such as acetylcholine, a short-acting stimulator of the release of endothelium-derived nitric oxide, has been used. Conversely, N-mono-methyl-l-arginine, a specific inhibitor of nitric oxide synthesis from l-arginine, has recently been shown to decrease blood flow during infusion into the brachial artery of healthy volunteers (control subjects) by inhibiting the basal release of nitric oxide. Consistent with experimental studies, the blood flow response to acetylcholine is blunted in patients with chronic heart failure compared with healthy age-matched volunteers. In contrast, the decrease in blood flow induced by N-mono-methyl-l-arginine appears to be exaggerated in congestive heart failure. The blood flow response to nitroglycerin or sodium nitroprusside, endothelium-independent vasodilators, is usually preserved in patients with chronic, nonedematous heart failure, indicating a normal response of the vascular smooth muscle of resistance vessels to exogenous nitric oxide. In contrast, the dilator response of the radial artery diameter to nitroglycerin and flow-dependent dilation is impaired in patients with chronic heart failure, indicating that the abnormal flow-mediated relaxation of large arteries may be caused by both endothelial and structural abnormalities. Thus impaired endothelium-dependent dilation of peripheral resistance vessels emerges in chronic heart failure, suggesting a reduced release of nitric oxide on stimulation; the latter (defective) mechanism may be involved in the impaired vasodilator capacity in the peripheral circulation (e.g., during exercise). In contrast, the basal release of nitric oxide from endothelium of resistance vessels appears to be preserved or may even be enhanced and may play an important compensatory role in chronic heart failure during resting conditions by antagonizing neurohumoral vasoconstrictor forces.

Original languageEnglish (US)
Pages (from-to)761-764
Number of pages4
JournalAmerican Heart Journal
Issue number3 PART 2
StatePublished - Sep 1993

All Science Journal Classification (ASJC) codes

  • Cardiology and Cardiovascular Medicine


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