L-Arginine availability determines the duration of acetylcholine-induced systemic vasodilatation in vivo Academic Article Article uri icon

Overview

MeSH Major

  • Fasciotomy
  • Prostatectomy
  • Prostatic Neoplasms
  • Suture Techniques
  • Therapeutic Irrigation

abstract

  • In vitro studies have shown that acetylcholine-induced vasorelaxation is mediated by endothelium-derived relaxing factor/nitric oxide (EDRF/NO). EDRF/NO is synthesized from L-arginine by an enzymatic pathway that is inhibited by L-NG-methylarginine. To assess whether EDRF/NO also mediates the vasodilating action of acetylcholine in vivo, we have investigated the effect of L-arginine and L-NG-methylarginine on the hypotensive response to acetylcholine in the anesthetized guinea pig. L-arginine prolonged the duration of the depressor response to acetylcholine and L-NG-methylarginine decreased it. However, neither L-arginine nor L-NG-methylarginine modified the magnitude of acetylcholine's hypotensive effect unless the blood pressure was previously elevated by infusion with norepinephrine. Thus, de novo synthesis of nitric oxide from L-arginine contributes importantly, but not exclusively, to acetylcholine's hypotensive effect in the guinea pig. Furthermore, the concentration of circulating L-arginine may influence the duration and magnitude of acetylcholine-induced depressor responses under normotensive and hypertensive conditions.

publication date

  • September 15, 1989

Research

keywords

  • Academic Article

Identity

Digital Object Identifier (DOI)

  • 10.1016/0006-291X(89)92281-X

PubMed ID

  • 2783117

Additional Document Info

start page

  • 710

end page

  • 7

volume

  • 163

number

  • 2