Pulmonary Vasodilator Response to Vagal Stimulation Is Blocked byNω‐Nitro‐l‐arginine Methyl Ester in the Cat
作者:
T. McMahon,
J. Hood,
P. Kadowitz,
期刊:
Circulation Research
(OVID Available online 1992)
卷期:
Volume 70,
issue 2
页码: 364-369
ISSN:0009-7330
年代: 1992
出版商: OVID
关键词: endothelium-derived relaxing factor;nitric oxide;neurogenic responses;cholinergic vasodilation;pulmonary vascular bed
数据来源: OVID
摘要:
The effect ofNω-nitro-l-arginine methyl ester (l-NAME), an inhibitor of endothelium-derived relaxing factor production, on the vasodilator response to efferent vagal stimulation was investigated in the pulmonary vascular bed of the intact-chest cat under conditions of controlled blood flow and constant left atrial pressure. When pulmonary vascular tone was increased with U46619, efferent vagal stimulation decreased lobar arterial pressure in a stimulus-frequency-dependent manner. The decreases in lobar arterial pressure were enhanced by pretreatment with reserpine, were blocked by atropine, and were not altered by propranolol, indicating that the neurogenic vasodilator response was cholinergic in nature. The decreases in lobar arterial pressure in response to vagal stimulation and to exogenously administered acetylcholine were reduced after administration of L-NAME (100 mg/kg i.v.). Although l-NAME decreased pulmonary vasodilator responses to vagal stimulation and to acetylcholine, responses to adenosine, nicorandil, lemakalim, isoproterenol, prostaglandin E1, sodium nitroprusside, and 8-bromo-cGMP, agents that act by a variety of mechanisms, were not decreased. These results are consistent with the hypothesis that efferent vagal stimulation releases acetylcholine, which dilates the pulmonary vascular bed by stimulating the production of nitric oxide or a labile nitroso compound from l-arginine.
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