© 1999 American Heart Association, Inc.
Original Contribution |
Potential Role of a Membrane-Bound NADH Oxidoreductase in Nitric Oxide Release and Arterial Relaxation to Nitroprusside
From the Department of Physiology, New York Medical College, Valhalla, NY.
Correspondence to Michael S. Wolin, PhD, Department of Physiology, New York Medical College, Valhalla, NY 10595. E-mail mike_wolin{at}nymc.edu
Abstract—The site of
metabolism in vascular smooth muscle responsible for the
release of nitric oxide (NO) from nitroprusside is not well
established. In this study we observed that a membrane-bound NADH
oxidoreductase in the pulmonary artery activates
nitroprusside to release NO, and we examined whether this process could
potentially participate in relaxation to nitroprusside. Relaxation to
nitroprusside in bovine calf pulmonary artery is inhibited by a
scavenger of NO and by an antagonist of NO stimulation of
guanylate cyclase. A flavoprotein probe that inhibits
pulmonary artery NADH oxidoreductase (1 µmol/L
diphenyliodonium) and electron acceptors for NADH oxidoreductase
(0.3 mmol/L nitroblue tetrazolium and 0.1 mmol/L
ferricyanide) inhibited pulmonary artery relaxation to
nitroprusside, but not to nitroglycerin.
Pulmonary arteries were observed to promote the release of NO
from nitroprusside in vitro, and NO release was inhibited by the
presence of nitroblue tetrazolium, ferricyanide, and diphenyliodonium.
In homogenates of pulmonary arteries, NADH
(0.1 mmol/L) increased the release of NO from nitroprusside by
6-fold, whereas NADPH, mitochondrial substrates, and other redox
cofactors had minimal effects on NO release, and the action of NADH on
nitroprusside was inhibited by nitroblue tetrazolium, ferricyanide, and
diphenyliodonium. A membrane fraction enriched in NADH oxidoreductase
activity showed a NADH-dependent release of NO from nitroprusside;
nitroprusside caused NADH consumption, and it also inhibited the
NADH-dependent reduction of nitroblue tetrazolium. Thus, a
membrane-bound NADH oxidoreductase appears to contribute to the release
of NO from nitroprusside, but not nitroglycerin, in
calf pulmonary artery.
Key Words: electron transport • guanylate cyclase • nitric oxide • nitroprusside • redox
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