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低雄激素水平对大鼠阴茎海绵体中IKca和SKca3通道的影响。

Effect of low androgen levels on IKca and SKca3 channels in rat penile corpus cavernosum.

作者信息

Zhao Hu, Jiang Jun, Xia Jiyi, Jiang Rui

机构信息

Department of Urology, Affiliated Hospital, Southwest Medical University, Luzhou, China.

Department of thyroid Surgery, Affiliated Hospital, Southwest Medical University, Luzhou, China.

出版信息

Andrologia. 2018 Nov;50(9):e13075. doi: 10.1111/and.13075. Epub 2018 Jun 28.

DOI:10.1111/and.13075
PMID:29952429
Abstract

We investigated whether low androgen levels affected erectile function by regulating the expressions of intermediate-conductance Ca -activated K channel (IKca) and small-conductance Ca -activated K channel 3 (SKca3) in corpus cavernous of rats. Thirty-six healthy male SD rats were randomly divided into the 4-week control group, 4-week castration group, 4-week androgen replacement after castration group, 8-week control group, 8-week castration group and 8-week androgen replacement after castration group, respectively. The rats in the androgen replacement groups were subcutaneously injected with testosterone (3 mg/kg) every other day after castration. After 4 and 8 weeks, maximum intracavernous pressure/mean arterial pressure (ICP /MAP) was measured. Expressions of IKca, SKca3, endothelial nitric oxide synthase (eNOS) and P-eNOS in penile corpus cavernosum were detected. ICP /MAP decreased significantly in the castration groups as compared to the control groups and the androgen replacement groups (p < 0.01). mRNA expressions of IKca and SKca3 decreased significantly in the castration groups as compared to the control groups and androgen replacement groups (p < 0.01). Protein expressions of eNOS, P-eNOS, IKca and SKca3 in the castration groups were significantly reduced as compared to the control groups and androgen replacement groups (p < 0.01). Under low androgen levels, ICP /MAP can be reduced by down-regulating the expressions of SKca3 and IKca, inhibiting P-eNOS/eNOS and reducing eNOS bioactivity.

摘要

我们研究了低雄激素水平是否通过调节大鼠海绵体中中间电导钙激活钾通道(IKca)和小电导钙激活钾通道3(SKca3)的表达来影响勃起功能。将36只健康雄性SD大鼠随机分为4周对照组、4周去势组、4周去势后雄激素替代组、8周对照组、8周去势组和8周去势后雄激素替代组。雄激素替代组的大鼠在去势后每隔一天皮下注射睾酮(3mg/kg)。4周和8周后,测量海绵体内最大压力/平均动脉压(ICP /MAP)。检测阴茎海绵体中IKca、SKca3、内皮型一氧化氮合酶(eNOS)和磷酸化eNOS(P-eNOS)的表达。与对照组和雄激素替代组相比,去势组的ICP /MAP显著降低(p <0.01)。与对照组和雄激素替代组相比,去势组中IKca和SKca3的mRNA表达显著降低(p <0.01)。与对照组和雄激素替代组相比,去势组中eNOS、P-eNOS、IKca和SKca3的蛋白表达显著降低(p <0.01)。在低雄激素水平下,可通过下调SKca3和IKca的表达、抑制P-eNOS/eNOS并降低eNOS生物活性来降低ICP /MAP。

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