Aim: To investigate whether estrogen was involved in relaxation of rabbit cavernous smooth muscle. Methods: Relaxation response of the rabbit cavernous smooth muscles to 17β-estradiol (0.3, 3, 30 and 300 nmol/L) were...Aim: To investigate whether estrogen was involved in relaxation of rabbit cavernous smooth muscle. Methods: Relaxation response of the rabbit cavernous smooth muscles to 17β-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 (10μmol/L) or L-NAME (10μmol/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 17β-estradiol increased the Maxi-K channel activities. Conclusion: 17β-estradiol may be involved in relaxation of rabbit cavernous smooth muscles via a non genomic and NO independent mechanism. 17β-estradiol stimulates Maxi-K channel of the rabbit cavernous myocyte.展开更多
文摘Aim: To investigate whether estrogen was involved in relaxation of rabbit cavernous smooth muscle. Methods: Relaxation response of the rabbit cavernous smooth muscles to 17β-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 (10μmol/L) or L-NAME (10μmol/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 17β-estradiol increased the Maxi-K channel activities. Conclusion: 17β-estradiol may be involved in relaxation of rabbit cavernous smooth muscles via a non genomic and NO independent mechanism. 17β-estradiol stimulates Maxi-K channel of the rabbit cavernous myocyte.
