Enhanced basal nitric oxide production in heart failure: another failed counter-regulatory vasodilator mechanism?

Endothelial dysfunction in heart failure could impair nitric oxide production and lead to increased vascular resistance. If endogenous production of nitric oxide is reduced, N G- monomethyl-L-arginine (L-NMMA), an inhibitor of such production, should have a diminished vasoconstrictor effect. We admi...

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Bibliographic Details
Published in:The Lancet (British edition) 1994-08, Vol.344 (8919), p.371-373
Main Authors: Habib, F., Dutka, D., Crossman, D., Oakley, C.M., Cleland, J.G.F.
Format: Article
Language:English
Subjects:
Aged
Arginine - analogs & derivatives
Arginine - pharmacology
Arginine - therapeutic use
Cardiac Output, Low - drug therapy
Cardiac Output, Low - metabolism
Cardiovascular disease
Female
Heart Failure - drug therapy
Heart Failure - metabolism
Heart Function Tests
Hemodynamics - drug effects
Hemodynamics - physiology
Humans
Male
Medical research
Middle Aged
Nitric Oxide - antagonists & inhibitors
Nitric Oxide - biosynthesis
Nitric Oxide - pharmacology
Nitric Oxide - physiology
Nitric Oxide - therapeutic use
omega-N-Methylarginine
Vasodilation - drug effects
Vasodilation - physiology
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Summary:Endothelial dysfunction in heart failure could impair nitric oxide production and lead to increased vascular resistance. If endogenous production of nitric oxide is reduced, N G- monomethyl-L-arginine (L-NMMA), an inhibitor of such production, should have a diminished vasoconstrictor effect. We administered L-NMMA to 12 patients being investigated for heart failure. L-NMMA increased median pulmonary and systemic vascular resistances by 61 (range - 3 to 240) and 430 (63 to 1609)dynes s cm -5, respectively (p
ISSN:0140-6736
1474-547X
DOI:10.1016/S0140-6736(94)91402-8