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Effect of low androgen levels on IK ca and SK ca3 channels in rat penile corpus cavernosum
Author(s) -
Zhao Hu,
Jiang Jun,
Xia Jiyi,
Jiang Rui
Publication year - 2018
Publication title -
andrologia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.633
H-Index - 59
eISSN - 1439-0272
pISSN - 0303-4569
DOI - 10.1111/and.13075
Subject(s) - castration , enos , androgen , endocrinology , medicine , testosterone (patch) , nitric oxide synthase , nitric oxide , hormone
We investigated whether low androgen levels affected erectile function by regulating the expressions of intermediate‐conductance Ca 2+ ‐activated K + channel (IKca) and small‐conductance Ca 2+ ‐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 max / MAP ) was measured. Expressions of IK ca, SK ca3, endothelial nitric oxide synthase ( eNOS ) and P‐ eNOS in penile corpus cavernosum were detected. ICP max / MAP decreased significantly in the castration groups as compared to the control groups and the androgen replacement groups ( p  < 0.01). mRNA expressions of IK ca and SK ca3 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 , IK ca and SK ca3 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 max / MAP can be reduced by down‐regulating the expressions of SK ca3 and IK ca, inhibiting P‐ eNOS / eNOS and reducing eNOS bioactivity.

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