PMID: 8945924Nov 1, 1996Paper

Exogenous NO inhibits basal NO release from vascular endothelium in vitro and in vivo

The American Journal of Physiology
X L MaJ Vinten-Johansen

Abstract

This study tested the hypothesis that exogenous nitric oxide (NO) inhibits basal release of NO in isolated rat aortic rings and in vivo. Thoracic aortic rings were suspended in organ chambers with Krebs-Henseleit solution. In untreated rings, the NO synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME) markedly increased basal vascular tone by 34.6 +/- 5.2% of maximal force produced by 100 nM thromboxane A2 mimetic U-46619, indicating a basal release of NO. Other rings were pretreated with the exogenous NO donor S-nitroso-N-acetylpenicillamine (SNAP) for 20 min and then washed free of drug. In these rings, L-NAME-induced vasoconstriction was significantly attenuated in a concentration-dependent manner (from 34.6 +/- 5.2 to 25.7 +/- 2.9% at SNAP = 0.5 microM, 15.2 +/- 3.1% at 1 microM, and 11.9 +/- 2.5% at 5 microM), while having no effect on NO-independent phenylephrine-induced vasoconstriction (35.4 +/- 4.7 untreated vs. 41.3 +/- 4.3% SNAP pretreated, not significant). In addition, the nonnitrosylated parent molecule of SNAP, acetylpenicillamine, had no effect on the vasoconstriction induced by L-NAME. In the in vivo studies in anesthetized rats, L-NAME caused significant hypertensive responses (34 +/- 4-mmHg increase i...Continue Reading

Citations

Oct 9, 2004·American Journal of Physiology. Heart and Circulatory Physiology·Seiichi MochizukiFumihiko Kajiya
Apr 25, 2000·American Journal of Physiology. Heart and Circulatory Physiology·N C GocanK Tyml
Jun 17, 2004·American Journal of Physiology. Renal Physiology·Xiaoling SuRobert S Moreland
Feb 13, 2001·American Journal of Physiology. Heart and Circulatory Physiology·X L MaT Yue
May 6, 2003·European Journal of Pharmacology·Chien Ming HuYu Wen Cheng

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