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Am J Physiol Regul Integr Comp Physiol 281: R476-R483, 2001;
0363-6119/01 $5.00
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Vol. 281, Issue 2, R476-R483, August 2001

Endothelin-1-induced vasoconstriction is inhibited during erection in rats

T. M. Mills1,2, D. M. Pollock1,3, R. W. Lewis2, H. S. Branam1, and C. J. Wingard1,3

Departments of 1 Physiology and of 2 Surgery (Urology Section), 3 Vascular Biology Center, Medical College of Georgia, Augusta, Georgia 30912-3000

Recent evidence indicates that endothelin-1 (ET-1) might be a principal vasoconstrictor in the penis. We report that ET-1 injection into the cavernous sinuses before erection sharply reduced the magnitude of subsequent erections. Corpus cavernosum pressure-to-mean arterial pressure ratios (CCP/MAP), with maximal ganglionic stimulation, were 0.62 ± 0.05 before ET-1 injection and 0.31 ± 0.05 after, indicating that ET-1 acted as a vasoconstrictor. When ET-1 was injected during a maximal neurally induced erection, the ability of ET-1 to attenuate subsequent erections was diminished (CCP/MAP 0.75 ± 0.02 before ET-1, 0.61 ± 0.03 after). At submaximal stimulation voltages, injection of ET-1 during erection also attenuated its vasoconstrictive effect. Similarly, when ET-1 was injected during erection induced by intracavernosal injection of the nitric oxide (NO) donor NOR-1, subsequent erections were not significantly suppressed (CCP/MAP 0.53 ± 0.04 before ET-1, 0.45 ± 0.04 after). These findings that ET-1-induced vasoconstriction is attenuated during erection are consistent with the hypothesis that NO mediates erection both by initiating pathways that cause smooth muscle relaxation and by inhibiting the vasoconstrictive actions of ET-1.

smooth muscle relaxation; nonadrenergic noncholinergic stimulation; nitric oxide donors


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