Circulation, Vol 85, 1894-1898, Copyright © 1992 by American Heart Association
A Lerman, EK Sandok, FL Hildebrand Jr and JC Burnett Jr
BACKGROUND. The endothelium possesses the ability to modulate vascular tone
by the release of vasodilators and vasoconstrictors, among them
endothelium-derived relaxing factor (EDRF) and endothelin (ET).
Abnormalities in EDRF generation have been demonstrated in various
cardiovascular pathophysiological states. Moreover, a twofold increase in
plasma ET concentration was reported in these disease states. Recent in
vitro studies have suggested the interaction between these two
endothelium-derived substances, suggesting that imbalance between the two
may contribute to alternation in vascular tone characteristic of these
disease states. Thus, the hypothesis of this study was that inhibition of
endogenous EDRF will enhance the vasoconstrictor response to a twofold
increase in plasma ET concentrations. METHODS AND RESULTS. Experiments were
conducted in three groups of anesthetized dogs. In group 1, ET-1 was
infused intravenously to double circulating ET concentrations. Group 2
received both ET and NG-monomethyl L-arginine (L-NMMA), a competitive
inhibitor of EDRF generation, and group 3 received a continuous infusion of
L-NMMA alone. Twofold increase in plasma ET concentrations was
characterized by an increase in systemic and renal vasoconstriction. The
inhibition of EDRF markedly enhanced the vasoconstriction to ET
specifically involving the systemic, pulmonary, coronary, and renal
arterial circulations. CONCLUSIONS. The present study demonstrates that
inhibition of endogenous EDRF augments the vasoconstrictor property of ET
and supports a functional role for the balance between endothelium-derived
vasodilating and vasoconstricting factors in the regulation of vascular
tone.
ARTICLES
Inhibition of endothelium-derived relaxing factor enhances endothelin- mediated vasoconstriction
Department of Internal Medicine, Mayo Clinic and Foundation, Rochester, Minn. 55905.
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