MONKEY CORPUS CAVERNOSUM RELAXATION MEDIATED BY NO AND OTHER RELAXINGFACTOR DERIVED FROM NERVES

Isolated monkey corpus cavernosum muscle strips contracted with prosta glandin F-2 alpha and treated with prazosin responded to transmural el ectrical stimulation with frequency-related relaxations that were abol ished by tetrodotoxin. The nitric oxide (NO) synthase inhibitor N-G-ni tro-L-arginine (L-NNA) significantly attenuated but did not abolish th e response; L-arginine reversed the inhibition. The neurogenic relaxat ion was not influenced in the strips treated with atropine or calciton in gene-related peptide (CGRP)-(8-37), a CGRP-receptor antagonist, and those desensitized to vasoactive intestinal polypeptide (VIP) or pitu itary adenylate cyclase-activating polypeptide (PACAP). Nerve fibers c ontaining NADPH diaphorase were histochemically demonstrated in cavern ous tissues. The relaxant response resistant to the NO synthase inhibi tor was abolished by high K+ and tetrabutylammonium but was unaffected by glibenclamide, charybdotoxin, apamin, ouabain, SKF-525a, a cytochr ome P-450 inhibitor, and oxyhemoglobin. It is concluded that neurogeni c relaxations of monkey corpus cavernosum muscle is associated partly with NO released as a neurotransmitter and that other relaxing factor( s) possibly responsible for K+ channel opening also participates; howe ver, the type of K+ channel involved is not determined. Acetylcholine, VIP, CGRP, PACAP, and the Na+ pump do not seem to be involved in the neurogenic relaxation.