作者: Xin‐hua Zhang , Arnold Melman , Michael E. DiSanto
DOI: 10.1111/J.1743-6109.2011.02218.X
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摘要: ABSTRACT Introduction Normal erectile function (EF) involves a coordinated relaxation of the arteries that supply penis and corpus cavernosum smooth muscle (CCSM), resulting in expansion sinusoids increased intracavernous pressure. But CCSM spends majority its time contracted state which is mediated by norepinephrine released from nerve endings other vasoconstrictors like endothelins endothelium. These agents cause myosin (SMM) phosphorylation elevating intracellular calcium. When calcium returns to basal levels, sensitivity increases prevents dephosphorylation, RhoA/Rho‐kinase (ROK) mechanism, thus maintaining force. Although mounting evidences demonstrate androgens have major influence on EF not just centrally mediated, this notion remains quite controversial. Aim To summarize current knowledge contractile pathways, role they play modulating EF, androgens. Methods The article reviews literature contains some previously unpublished data contraction signaling including are known these pathways. Main Outcome Measures Data peer‐reviewed publications observations. Results In addition downregulation many pro‐erectile molecular mechanisms, decreased testosterone (T) levels upregulate contractility, hyperresponsiveness α‐adrenergic agonists, SMM phosphorylation, alteration isoform composition, activation RhoA/ROK modulation sphingosine‐1‐phosphate regulation tone. Conclusions Decreased T signaling. Meanwhile, it downregulates pathways synergizing produce dysfunction (ED). urologists researchers still skeptical penile erection, understanding control mechanisms as well should provide new evidence supporting roles enhance discovery novel targets for drug development treat ED. Zhang X, Melman A, DiSanto ME. Update function: A testosterone? J Sex Med 2011;8:1865–1879.