NDLI: Pulmonary vasodilator responses to sodium nitrite are mediated by an allopurinol-sensitive mechanism in the rat

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Casey, David B. Badejo, Adeleke M. Dhaliwal, Jasdeep S. Murthy, Subramanyam N. Hyman, Albert L. Nossaman, Bobby D. Kadowitz, Philip J.
Description	Country affiliation: United States Author Affiliation: Casey DB ( Department of Pharmacology, Tulane University Health Sciences Center, New Orleans, LA, USA.)
Abstract	Recent studies show that pulmonary vasodilator responses to nitrite are enhanced by hypoxia. However, the mechanism by which nitrite is converted to vasoactive nitric oxide (NO) is uncertain. In the present study, intravenous injections of sodium nitrite decreased pulmonary and systemic arterial pressures and increased cardiac output. The decreases in pulmonary arterial pressure were enhanced when tone in the pulmonary vascular bed was increased with U-46619. Under elevated tone conditions, decreases in pulmonary and systemic arterial pressures in response to nitrite were attenuated by allopurinol in a dose that did not alter responses to the NO donors, sodium nitroprusside and diethylamine/NO, suggesting that xanthine oxidoreductase is the major enzyme-reducing nitrite to NO. Ventilation with a 10% $O_{2}$ gas mixture increased pulmonary arterial pressure, and the response to hypoxia was enhanced by $N^{G}-nitro-l-arginine$ methyl ester and not altered by allopurinol. This suggests that NO formed by the endothelium and not from the reduction of plasma nitrite modulates the hypoxic pulmonary vasoconstrictor response. Although intravenous injections of sodium nitrite reversed pulmonary hypertensive responses to U-46619, hypoxia, and $N^{G}-nitro-l-arginine$ methyl ester, the pulmonary vasodilator response to nitrite was not altered by ventilation with 10% $O_{2}$ when baseline pulmonary arterial pressure was increased to similar values in animals breathing room air or the hypoxic gas. These data provide evidence that xanthine oxidoreductase is the major enzyme-reducing nitrite to vasoactive NO, and that this mechanism is not modified by hypoxia.
File Format	HTM / HTML
ISSN	03636135
e-ISSN	15221539
DOI	10.1152/ajpheart.00543.2008
Journal	AJP: Heart and Circulatory Physiology
Issue Number	2
Volume Number	296
Language	English
Publisher	American Physiological Society
Publisher Date	2009-02-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Discipline Physiology Discipline Cardiology Allopurinol Pharmacology Enzyme Inhibitors Nitric Oxide Metabolism Pulmonary Artery Drug Effects Sodium Nitrite Vasodilation Vasodilator Agents Xanthine Oxidase Antagonists & Inhibitors 15-hydroxy-11 Alpha,9 Alpha-(epoxymethano)prosta-5,13-dienoic Acid Animals Blood Pressure Cardiac Output Disease Models, Animal Dose-response Relationship, Drug Hydrazines Anoxia Enzymology Physiopathology Injections, Intravenous Ng-nitroarginine Methyl Ester Nitric Oxide Donors Nitric Oxide Synthase Nitroprusside Oxypurinol Rats, Sprague-dawley Administration & Dosage Time Factors Vasoconstrictor Agents Comparative Study Research Support, N.i.h., Extramural
Content Type	Text
Resource Type	Article
Subject	Physiology Physiology (medical) Cardiology and Cardiovascular Medicine

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