Endothelial nitric oxide synthase regulation in female genital tract structures.
Endothelial nitric oxide synthase regulation in female genital tract structures.
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DOI：
10.1111/j.1743-6109.2008.01122.x
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发表时间：
2009-03
期刊：
影响因子：
--
通讯作者：
Burnett AL
中科院分区：
文献类型：
--
作者：
Musicki B;Liu T;Lagoda GA;Bivalacqua TJ;Strong TD;Burnett AL
女性性唤起障碍（FSAD）是女性性功能障碍的主要组成部分，影响25-70%的女性。FSAD的机制知之甚少。雌激素有助于性反应期间生殖器血流的控制。雌激素的血管效应主要归因于其调节内皮一氧化氮（NO）的产生。然而，内皮型一氧化氮合酶（eNOS）的作用和机制，调节eNOS在女性生殖道结构在很大程度上是未知的。综述eNOS在女性生殖道结构中的调节机制。本文综述了NO和eNOS在女性性唤起中的作用及其受雌激素调节的相关文献。女性性唤起，NO和eNOS之间的关联。NO/环磷酸鸟苷途径被认为在性唤起期间调节阴蒂和阴道血流以及平滑肌松弛中具有主要作用。雌激素对于维持阴道和阴蒂的血流和阴道渗出液的产生至关重要。雌激素通过基因组机制和非基因组机制调节eNOS，基因组机制涉及增强的mRNA转录和蛋白质合成，而非基因组机制发生在基因表达无改变的情况下。然而，有限的研究已经评估了内皮NO的生理作用和eNOS调节女性生殖道的分子机制。雌激素增加生殖器血流量和平滑肌松弛的作用主要归因于eNOS的调节。然而，女性生殖道结构中eNOS调节的确切机制以及eNOS缺陷与衰老和血管疾病的分子基础需要进一步研究。
Female sexual arousal disorder (FSAD) is a major component of female sexual dysfunctions, affecting 25–70% of women. The mechanisms of FSAD are poorly understood. Estrogen contributes to the control of genital blood flow during the sexual response. Vascular effects of estrogen are mostly attributed to its regulation of endothelial nitric oxide (NO) production. However, the role of endothelial NO synthase (eNOS) and the mechanisms that regulate eNOS in female genital tract structures are largely unknown. To review available evidence of the mechanisms of eNOS regulation in female genital tract structures. This article reviews the literature that relates to the role of NO and eNOS in female sexual arousal and its modulation by estrogen. Association between female sexual arousal, NO, and eNOS. The NO/cyclic guanosine monophosphate pathway is believed to have a primary role in the regulation of clitoral and vaginal blood flow, and smooth muscle relaxation during sexual arousal. Estrogen is critical for maintaining vaginal and clitoral blood flow and vaginal transudate production. Estrogen regulates eNOS by genomic mechanisms, involving augmented mRNA transcription and protein synthesis, and by non-genomic mechanisms, which occur without alterations in gene expression. However, limited studies have evaluated the physiological role of endothelial NO and the molecular mechanisms of eNOS regulation in the female genital tract. The effects of estrogen on increasing genital blood flow and smooth muscle relaxation have been attributed mostly to regulation of eNOS. However, the exact mechanisms of eNOS regulation in female genital tract structures and the molecular basis for the eNOS defect with aging and vascular diseases warrant further investigation.
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