Endothelial dysfunction in chronic heart failure. Experimental and clinical studies

H. Drexler, D. Hayoz, T. Munzel, H. Just, Robert Zelis, H. R. Brunner

Research output: Contribution to journalArticle

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Abstract

The endothelium plays an important role in the control of human vascular tone by releasing endothelium-derived nitric oxide. Therefore, endothelial dysfunction could be involved in the increased peripheral vasoconstriction of patients with chronic congestive heart failure (CHF). To investigate endothelial function in humans in vivo, agents such as acetylcholine are used to stimulate the release of endothelium-derived nitric oxide (EDRF). Conversely, N-mono-methyl-L-arginine (L-NMMA), a specific inhibitor of nitric oxide synthesis from L-arginine decreases forearm blood flow 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 as compared to healthy age-matched volunteers. In contrast, the decrease in blood flow induced by L-NMMA appears to be exaggerated in CHF. The blood flow response to nitroglycerin or sodium nitroprusside, endothelium-independent vasodilators, is usually preserved in patients with chronic, non-edematous 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 are impaired in patients with chronic heart failure, indicating that the abnormal flow-mediated relaxation of large arteries may be due to both endothelial and vascular smooth muscle alterations. Thus, impaired endothelium-dependent dilation of peripheral resistance vessels emerges in chronic heart failure, suggesting a reduced release of nitric oxide upon stimulation. Thus, endothelial dysfunction 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 enhanced and may play an important compensatory role in chronic heart failure.

Original languageEnglish (US)
Pages (from-to)455-458
Number of pages4
JournalArzneimittel-Forschung/Drug Research
Volume44
Issue number3 A
StatePublished - Jan 1 1994

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Nitric Oxide
Heart Failure
Endothelium
Blood
omega-N-Methylarginine
Nitroglycerin
Vasodilator Agents
Vascular Smooth Muscle
Acetylcholine
Arginine
Muscle
Dilatation
Radial Artery
Nitroprusside
Clinical Studies
Vasoconstriction
Forearm
Vascular Resistance
Blood Vessels
Volunteers

All Science Journal Classification (ASJC) codes

  • Drug Discovery

Cite this

Drexler, H., Hayoz, D., Munzel, T., Just, H., Zelis, R., & Brunner, H. R. (1994). Endothelial dysfunction in chronic heart failure. Experimental and clinical studies. Arzneimittel-Forschung/Drug Research, 44(3 A), 455-458.
Drexler, H. ; Hayoz, D. ; Munzel, T. ; Just, H. ; Zelis, Robert ; Brunner, H. R. / Endothelial dysfunction in chronic heart failure. Experimental and clinical studies. In: Arzneimittel-Forschung/Drug Research. 1994 ; Vol. 44, No. 3 A. pp. 455-458.
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Drexler, H, Hayoz, D, Munzel, T, Just, H, Zelis, R & Brunner, HR 1994, 'Endothelial dysfunction in chronic heart failure. Experimental and clinical studies', Arzneimittel-Forschung/Drug Research, vol. 44, no. 3 A, pp. 455-458.

Endothelial dysfunction in chronic heart failure. Experimental and clinical studies. / Drexler, H.; Hayoz, D.; Munzel, T.; Just, H.; Zelis, Robert; Brunner, H. R.

In: Arzneimittel-Forschung/Drug Research, Vol. 44, No. 3 A, 01.01.1994, p. 455-458.

Research output: Contribution to journalArticle

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