NEUROGENIC CONTRACTION AND RELAXATION OF HUMAN PENILE DEEP DORSAL VEIN

1 The aim of the present study was to characterize neurogenic and phar macological responses of human penile deep dorsal vein and to determin e whether the responses are mediated by nitric oxide from neural or en dothelial origin. 2 Ring segments of human penile deep dorsal vein wer e obtained from 22 multiorgan donors during procurement of organs for transplantation. The rings were suspended in organ bath chambers for i sometric recording of tension. We then studied the contractile and rel axant responses to electrical field stimulation and to vasoactive agen ts. 3 Electrical held stimulation (0.5-2 Hz) and noradrenaline (3 x 10 (-10)-3 x 10(-5) M) caused frequency- and concentration-dependent cont ractions that were of greater magnitude in veins denuded of endotheliu m. The inhibitor of nitric oxide synthesis N-G-nitro-L-arginine methyl ester hydrochloride (L-NAME, 10(-4) M) increased the adrenergic respo nses only in rings with endothelium. 4 In preparations contracted with noradrenaline in the presence of guanethidine (10(-6) M) and atropine (10(-6) M), electrical stimulation induced frequency-dependent relaxa tions. This neurogenic relaxation was prevented by L-NAME, methylene b lue (3 x 10(-5) M) and tetrodotoxin (10(-6) M), but was unaffected by removal of endothelium. 5 Acetylcholine (10(-8)-3 x 10(-5) M) and subs tance P (3 x 10(-11)-3 x 10(-7) M) induced endothelium-dependent relax ations. In contrast, sodium nitroprusside (10(-9)-3 x 10(-5) M) and pa paverine (10(-8)-3 x 10(-5) M) caused endothelium-independent relaxati ons. The results provide functional evidence that the human penile dee p dorsal vein is an active component of the penile vascular resistance through the release of nitric oxide from both neural and endothelial origin. Dysfunction in any of these sources of nitric oxide should be considered in some forms of impotence.