ROLE OF THE L-ARGININE NITRIC-OXIDE PATHWAY IN RELAXATION OF ISOLATEDHUMAN PENILE CAVERNOUS TISSUE AND CIRCUMFLEX VEINS

In human penile corpus cavernosum strips, pre-contracted by noradrenal ine, electrical stimulation of nerves evoked non-adrenergic, non-choli nergic (NANC) relaxant responses which could be inhibited by tetrodoto xin 10(-6) m, N(G)-nitro-L-arginine (L-NNA) 10(-7)-10(-4) m, and oxyha emoglobin 10(-5) m, but not by methylene blue (MB) 10(-5) m. Acetylcho line-induced relaxations were also inhibited by L-NNA 10(-4) m and oxy haemoglobin 10(-5) m, but were unaffected by pyrogallol 10(-4) m, MB 1 0(-5) m, and tetrodotoxin 10(-6) m. MB 5 x 10(-4)-10(-4) M significant ly reduced the responses to both electrical stimulation and to acetylc holine. Nitric oxide (NO) 10(-7)-10(-4) m and sodium nitroprusside 10( -9)-10(-4) M caused concentration-dependent relaxations. The NO-induce d relaxations were inhibited by oxyhaemoglobin 10(-5) m, and the conce ntration-response curve for sodium nitroprusside was shifted to the ri ght by MB 10(-5) m. The response to sodium nitroprusside was unaffecte d by L-NNA 10(-4) m, oxyhaemoglobin 10(-5) m, and pyrogallol 10(-4) M. In circumflex veins, pre-contracted by noradrenaline, no NANC-mediate d relaxation was found in response to electrical stimulation; acetylch oline caused endothelium-dependent relaxations, which were insensitive to L-NNA 10(-4) M and oxyhaemoglobin 10(-5) m. NO and sodium nitropru sside caused concentration-dependent relaxations; the concentration-re sponse curves for NO and sodium nitroprusside were shifted to the righ t by oxyhaemoglobin 10(-5) m. Removal of the endothelium left the NO- and sodium nitroprusside-induced relaxations unchanged. The results co nfirm previous observations that relaxations of human corpus cavernosu m induced by both NANC nerve stimulation and exogenous acetylcholine i nvolve an agent derived froM L-arginine. No NANC response to electrica l stimulation was found in circumflex veins, where acetylcholine induc ed an endothelium-dependent relaxation, apparently independent of the L-arginine/nitric oxide pathway.