The Role of Prostanoids in vivo Feline Penile Erection

Moon, Du Geon; Kim, Young Don; Koh, Sung Kun; Kim, Je Jong

Abstract

PURPOSE
The widespread use of intracorporeal prostaglandin E1 (PGE 1) injection for the treatment of erectile dysfunction has focused interest on the physiological functions of prostanoids with the mechanism of action. We investigated in vivo feline penile erectile and contractile responses to prostanoids.
MATERIALS AND METHODS
Under the general anesthesia, 26 mature male cats were conditioned normoxia and hypoventilated hypoxia with ventilator in room air(PH: 7.14+/- 0.47, PO2: 25.52+/-5.89mmHg, PCO2: 74.27+/-10.86mmHg). Vasoactive substances were infused via internal pudendal artery and the changes of intracavernous pressure to vasoactive substances were monitored with physiograph under normoxia and hypoxia with acidosis.
RESULTS
Under normoxia, PGE1 induced dose-dependent cavernous relaxation and PGE1 was more potent than papaverine but less than acetylcholine. PGE1- induced cavernous relaxation was blocked by the K+-channel blockers, tetraethylammonium(TEA) and 4-aminopyridine, in dose-dependent manner but was completely reversed by the K+-channel opener, pinacidil. Calcium ionophore, ionomycin(10-3M/0.2ml) prevented the cavernous relaxation by PGE1 under hypoxia(n=6, p<0.01). PGI2 showed minimal cavernous relaxation with tumescence. Thromboxane A2(TXA2) attenuated the acetylcholine-induced relaxation
CONCLUSIONS
This study showed that PGE2 relax feline cavernous smooth muscle. But the mechanism of PGE2 on feline cavernosum should be elucidated by the receptor binding study. These results suggest that PGE2 induced smooth muscle relaxation by the opening of Maxi-K+ (Kca) channel and subsequent hyperpolarization. It would be followed by a reduced opening of voltage-dependent Ca2+-channel and subsequent decrease of intracellular Ca2+concentration.