Monkey corpus cavernosum relaxation mediated by NO and other relaxing factor derived from nerves

Abstract

Isolated monkey corpus cavernosum muscle strips contracted with prostaglandin F(2α) and treated with prazosin responded to transmural electrical stimulation with frequency-related relaxations that were abolished by tetrodotoxin. The nitric oxide (NO) synthase inhibitor N(G)-nitro-L- arginine (L-NNA) significantly attenuated but did not abolish the response; L-arginine reversed the inhibition. The neurogenic relaxation was not influenced in the strips treated with atropine or calcitonin gene-related peptide (CGRP)-(8-37), a CGRP-receptor antagonist, and those desensitized to vasoactive intestinal polypeptide (VIP) or pituitary adenylate cyclase- activating polypeptide (PACAP). Nerve fibers containing NADPH diaphorase were histochemically demonstrated in cavernous tissues. The relaxant response resistant to the NO synthase inhibitor was abolished by high K+ and tetrabutyl-ammonium but was unaffected by glibenclamide, charybdotoxin, apamin, ouabain, SKF-525a, a cytochrome P-450 inhibitor, and oxyhemoglobin. It is concluded that neurogenic 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; however, 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.