No abstract

The severity of the neurological disease is the only predictive factor for the occurrence of voiding dysfunction, which affects men and women alike.

To elucidate the neuropharmacology of erection, we undertook an in vivo canine study to examine the role of cholinergic and nonadrenergic, noncholinergic (NANC) neuroeffectors and the sinusoidal endothelium in erection induced by electrostimulation. We also examined the effect of adenylate cyclase and guanylate cyclase blockers by intravenous injection of N-ethylmaleimide and methylene blue, respectively. In addition, the effects of intracavernous injection of the nitric oxide-releasing substance, nitroprusside, and bromocyclic adenosine monophosphate (AMP) and bromocyclic guanosine monophosphate (GMP) were also studied. In contrast to in vitro results, atropine reduced the increase of intracavernous pressure after neurostimulation (p = 0.029). Intracavernous injection of CHAPS to destroy the sinusoidal endothelium abolished the response to acetylcholine (p = 0.001), but only partially inhibited the response to electrostimulation (mean = 75% pressure increase, p = 0.022), indicating that neuronal nitric oxide plays a major role in penile erection. Methylene blue, a guanylate cyclase inhibitor, significantly inhibited the erectile response to both neurostimulation and sodium nitroprusside (p = 0.000 and 0.017, respectively). However, N-ethylmaleimide, an adenylate cyclase inhibitor, could not reduce the response to neurostimulation (p = 0.078). The erectile response to intracavernous injection of cGMP was significantly better than that induced by cAMP (p = 0.025). Our results suggest that both the cholinergic and NANC neuroeffectors and the sinusoidal endothelium are involved in erection. In addition, our data imply that the neuronal nitric oxide/cyclic GMP system is the most likely pathway for penile smooth muscle relaxation and erection.

No abstract

We sought to determine whether the L-arginine-nitric oxide-guanosine 3',5'-cyclic monophosphate (cGMP) pathway, known to mediate neurostimulation-induced smooth muscle relaxation in penile tissue of rabbits and humans in vitro, is operative also in vivo. Adult male dogs (n = 9) were subjected to direct electrical stimulation of the pelvic nerves to induce penile tumescence. Intracavernous injection of the nitric oxide-releasing substance S-nitroso-N-acetylpenicillamine resulted in similar tumescence. Intracavernous injection of a specific inhibitor of nitric oxide synthesis, NG-nitro-L-arginine, blocked pelvic nerve-stimulated tumescence, and this was partially reversed by intracavernous injection of the nitric oxide precursor L-arginine. Furthermore, neurostimulated tumescence was inhibited by methylene blue, an inhibitor of cytosolic guanylate cyclase and enhanced by M&B 22948, a cGMP phosphodiesterase inhibitor. These in vivo findings support the hypothesis that cavernous smooth muscle relaxation and penile tumescence are mediated by nitric oxide and cGMP.