The hypotensive action of acetylcholine in vivo may be dependent on the release of the novel vasorelaxant, endothelium-derived relaxing factor (EDRF)/nitric oxide (NO), by the vascular endothelium. However, using two different inhibitors of NO synthesis, NG-monomethyl-L-arginine (L-NMMA, 100 mg/kg) and NG-nitro-L-arginine methyl ester (L-NAME, 100 mg/kg), we have been unable to attenuate the hypotensive action of intravenous (i.v.) boluses of acetylcholine in anesthetized rats. L-NMMA also failed to alter the hypotensive effect of i.v. bradykinin and adenosine triphosphate (ATP). NO generation by a column of cultured endothelial cells was, however, completely abolished by L-NMMA. The hypotensive effect of acetylcholine was not affected by glibenclamide at a dose which blocks the effect of i.v. cromakalim, a drug which opens ATP-sensitive K+ channels. The rapid hypotensive response to i.v. bolus acetylcholine, ATP and bradykinin remains unexplained.

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