Role of adenosine triphosphate-dependent potassium channels in canine penile erection

To define the physiologic role and hemodynamic features of nitric oxide (NO) and the adenosine triphosphate (ATP)-dependent K(+) (K(ATP)) channel in canine penile erection.

Mongrel dogs were anesthetized, and penile erection was induced by electrical stimulation of the pelvic nerve. Changes in the intracavernous pressure (ICP) were measured with a transducer.

The basal ICP was 12.8 +/- 5.0 mm Hg. Pelvic nerve stimulation (5 to 20 V, 5 to 15 Hz, for 1-minute intervals) significantly increased the ICP to 86.2 +/- 11.4 mm Hg (n = 5, P <0.05). Treatment with the NO synthase inhibitor N(omega)-nitro-L-arginine methyl ester (10 mg/kg intravenously) abolished this increase (15.4 +/- 5.0 mm Hg, n = 5). Intracavernous injection of the K(ATP) channel opener cromakalim (3 and 10 microg) increased the ICP (103 +/- 14.4 mm Hg and 106 +/- 12.1 mm Hg, respectively; n = 4). This response was abolished by the prior intracavernous injection of the selective K(ATP) channel-specific blocker glibenclamide (10 mg). Glibenclamide did not affect the increase in ICP induced by electric stimulation of the pelvic nerve (88 +/- 24.2 mm Hg).

Our results indicate that relaxation of canine cavernous smooth muscle and penile tumescence are mediated by NO. The failure of glibenclamide to affect the increase in ICP induced by pelvic nerve stimulation suggests that ATP-dependent K(+) channels probably do not play a physiologic role in canine penile erection.