PMID: 8945907Nov 1, 1996Paper

Nitric oxide inhibits pulmonary artery catalase and H2O2-associated relaxation

The American Journal of Physiology
K M Mohazzab-HMichael S Wolin

Abstract

Our previous studies on the mechanism of relaxation of calf pulmonary arteries to H2O2 detected a role for increased formation of guanosine-3',5'-cyclic monophosphate as a result of a catalase-elicited activation of soluble guanylate cyclase. We have also shown that lactate elicits relaxation through increasing H2O2 produced from NADH oxidase-derived superoxide anion (O2-.). Because nitric oxide (NO) is a potential inhibitor of catalase, we examined the effects of exposure of endothelium-denuded bovine calf pulmonary arteries to an elevated physiological level of NO on relaxation to H2O2 and lactate. Treatment of pulmonary arteries with approximately 50 nM of NO gas for 2 min caused a subsequent inhibition of relaxation to H2O2 (10(-6) to 10(-3)M) and lactate (1-10 mM), without markedly altering relaxation responses to S-nitroso-N-acetylpenicillamine (10(-9) to 10(-6) M) or isoproterenol (10(-9) to 10(-6) M). This NO exposure caused a 63 and 70% inhibition of the metabolism by smooth muscle catalase of both endogenously produced and exogenous (100 microM) H2O2, respectively, as measured by the H2O2-dependent cooxidation of methanol to formaldehyde. A similar treatment of purified catalase with NO caused subsequent inhibition of...Continue Reading

Citations

Jul 9, 2005·American Journal of Physiology. Lung Cellular and Molecular Physiology·Michael S WolinSachin A Gupte
Jan 20, 2009·American Journal of Physiology. Heart and Circulatory Physiology·Michael S Wolin
Mar 10, 2000·American Journal of Physiology. Heart and Circulatory Physiology·R FigueroaM S Wolin

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