SUPPRESSION BY NG-MONOMETHYL-L-ARGININE OF CEREBROARTERIAL RESPONSES TO NONADRENERGIC, NONCHOLINERGIC VASODILATOR NERVE-STIMULATION

Relaxations caused by electrical and chemical (nicotine) stimulation of nonadrenergic, noncholinergic nerves are not influenced in dog cerebral arteries made tachyphylactic to peptides, such as vasoactive intestinal polypeptide (VIP), calcitonin gene-related peptide (CGRP), and atrial natriuretic peptide (ANP), but are abolished by oxyhemoglobin and methylene blue. Treatment with N(G)-monomethyl-L-arginine (L-NMMA), a nitric oxide (NO) synthesis inhibitor, suppresses the relaxant response to vasodilator nerve stimulation, whereas D-NMMA is ineffective. L-arginine, but not D-arginine, prevents or reverses the inhibitory effect Of L-NMMA. NO or a NO-related compound appears to play a quite important role in the neurotransmission in vasodilator nerves innervating the cerebral arterial wall.