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Volume 6, Issue 2 (June 2004) 6, 127–131;
Relaxation of rabbit cavernous smooth muscle to 17b-estradiol: a non-genomic, NO-independent mechanism
S.C. Kim, K.K. Seo, S.C. Myung, M.Y. Lee
Department of Urology, 2Department of Physiology, College of Medicine, Chung-Ang University, Seoul 140-757, Korea
Advance online publication 1 June 2004
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Aim: To investigate whether estrogen was involved in relaxation of rabbit cavernous smooth muscle. Methods: Relaxation response of the rabbit cavernous smooth muscles to 17-estradiol (0.3, 3, 30 and 300 nmol/L) were observed in vitro. The response of the muscle strips to estrogen after incubation with either actinomycin D (10 mol/L) or L-NAME (10 mol/L) were also evaluated. Inside-out mode of patch clamp in a single smooth muscle cell was applied to investigate the Maxi-K channel activities. Results: Estrogen caused a dose-dependent relaxation of the strips precontracted with norepinephrine. The maximal response was noted about 10 minutes after treatment. The estrogen-induced relaxation was prevented by neither actinomycin D nor L-NAME, suggesting that the response was not mediated by gene transcription or nitric oxide (NO). Application of 17-estradiol increased the Maxi-K channel activities. Conclusion: 17-estradiol may be involved in relaxation of rabbit cavernous smooth muscles via a non-genomic and NO independent mechanism. 17-estradiol stimulates Maxi-K channel of the rabbit cavernous myocyte.
Aim: To investigate whether estrogen was involved in relaxation of rabbit cavernous smooth muscle. Methods: Relaxation response of the rabbit cavernous smooth muscles to 17-estradiol (0.3, 3, 30 and 300 nmol/L) were observed in vitro. The response of the muscle strips to estrogen after incubation with either actinomycin D (10 mol/L) or L-NAME (10 mol/L) were also evaluated. Inside-out mode of patch clamp in a single smooth muscle cell was applied to investigate the Maxi-K channel activities. Results: Estrogen caused a dose-dependent relaxation of the strips precontracted with norepinephrine. The maximal response was noted about 10 minutes after treatment. The estrogen-induced relaxation was prevented by neither actinomycin D nor L-NAME, suggesting that the response was not mediated by gene transcription or nitric oxide (NO). Application of 17-estradiol increased the Maxi-K channel activities. Conclusion: 17-estradiol may be involved in relaxation of rabbit cavernous smooth muscles via a non-genomic and NO independent mechanism. 17-estradiol stimulates Maxi-K channel of the rabbit cavernous myocyte.
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