Inhibitory effects of L-N G-nitro-arginine on the synthesis of EDRF and the cerebroarterial response to vasodilator nerve stimulation

Abstract

Treatment with L-N G-nitro-arginine (L-NA) inhibited the bradykinin-induced relaxation, mediated via EDRF, in dog coronary artery strips partially contracted with prostaglandin F 2α; the inhibition was prevented by L-, but not D-, arginine. Relaxation caused by nitrogylycerin was not altered by L-NA. The release of EDRF, as assayed using dog coronary artery strips without endothelium, from perfused femoral artery segments with endothelium in response to acetylcholine and substance P was significantly reduced by treatment of the femoral artery with L-NA. The inhibitory effect was reversed by L-arginine. Relaxant responses of dog cerebral artery strips with and without endothelium to electrical stimulation of non-adrenergic, non-cholinergic nerves were suppressed by L-NA, whereas relaxation of coronary arteries with and without endothelium by the stimulation of adrenergic nerves was not influenced. The L-NA-induced inhibition was reversed by L-arginine. It is speculated that L-NA inhibits the synthesis of EDRF, as does L-N G-monomethyl arginine, and NO-like substance(s) produced plays an important role in transferring information from vasodilator nerves to smooth muscle in cerebral arteries.