Korean J Urol.
1993 Jun;34(3):431-438.
Experimental study of the role of nitric oxide of cavernous smooth muscle relaxation
- Affiliations
-
- 1Departmet of Urology, College of Medicine, Dong-A University, Pusan, Korea.
- 2Departmet of Urology, Cha's Urologic Cliric, Pusan, Korea.
Abstract
-
Relaxation of penile cavernous smooth muscle is controlled by nerve and endothelium derived substances. Externally applied acetylcholine in human corpus cavernosum has been shown to cause endothelium dependent smooth muscle relaxation and nitric oxide(NO) is known as an endothelium derived relaxing factor(EDRF). NO has been identified as an endothelium derived relaxing factor in blood vessels. We tried to determine whether it is involved in the relaxation of the corpus cavernosum that allows penile erection. The changes of isometric tension in rabbit cavernous smooth muscle strips mounted in organ bath chambers after the addition of drugs were monitored on the biophysical recording system. Acetylcholine induced a dose-dependent relaxation and atropine at 5 x 10(-5) M almost abolished the effects of acetylcholine. N(c)-nitro-L-arginine (L-NOARG) at 5 x 10(-5) M almost abolished the effects of acetylcholine. The subsequent addition of L-arginine at 5 x 10(-5) M further restored to the effect of acetylcholine, but these effect did not occur if D -arginine was substituted for L-arginine. Methylene blue at 10-5 M markedly inhibited effects of acetylcholine. These data suggest that acetylcholine endothelial formation of NO via muscarinic receptor and NO from L-arginine leads to the relaxation of cavernous smooth muscle via activation of guanylate cyclase in rabbit.