Min K, O'Connell L, Munarriz R, Huang Y H, Choi S, Kim N, Goldstein I, Traish A
Department of Urology, Boston University School of Medicine, MA 02118, USA.
Int J Impot Res. 2001 Jun;13(3):151-6. doi: 10.1038/sj.ijir.3900683.
There have been limited anatomic and physiological investigations of the female sexual arousal response. A broader understanding of the physiologic mechanisms of female sexual arousal function is required to improve the management of women with sexual dysfunction. Three experimental test systems have been developed to understand better the biochemical and physiological mechanisms of female sexual arousal response. An in vivo animal model was developed to record physiological and hemodynamic changes in the clitoris and vagina following pelvic nerve stimulation and administration of vasoactive agents and physiological modulators. In vitro organ baths of clitoral and vaginal tissue were utilized to investigate mechanisms involved in the regulation of smooth muscle contractility. In addition, primary cell cultures of human and animal clitoral and vaginal smooth muscle cells were developed to investigate signal transduction pathways modulating smooth muscle tone. In vivo studies revealed hemodynamic changes in vagina and clitoris in response to pelvic nerve stimulation, vasodilators and physiological modulators. Organ bath studies have demonstrated that clitoral and vaginal smooth muscle tone is affected by non-adrenergic and non-cholinergic neurotransmitters, and the presence of functional alpha 1 and alpha 2 adrenergic receptors in these tissues has been established through biochemical studies. These changes are regulated by the tone of vascular and non-vascular smooth muscle in the vagina and clitoris. Primary cell culture studies have suggested that several physiological modulators such as vasoactive intestinal polypeptide (VIP), nitric oxide (NO), and prostaglandin E (PGE) regulate vaginal smooth muscle contractility. Data from experimental models have provided a preliminary understanding of the mechanisms of the female sexual arousal response.
对女性性唤起反应的解剖学和生理学研究一直有限。为了改善性功能障碍女性的治疗，需要更广泛地了解女性性唤起功能的生理机制。已经开发了三种实验测试系统，以更好地理解女性性唤起反应的生化和生理机制。开发了一种体内动物模型，用于记录盆腔神经刺激以及给予血管活性药物和生理调节剂后阴蒂和阴道的生理和血流动力学变化。利用阴蒂和阴道组织的体外器官浴来研究参与平滑肌收缩调节的机制。此外，还建立了人和动物阴蒂及阴道平滑肌细胞的原代细胞培养体系，以研究调节平滑肌张力的信号转导途径。体内研究揭示了阴道和阴蒂对盆腔神经刺激、血管扩张剂和生理调节剂的血流动力学变化。器官浴研究表明，阴蒂和阴道的平滑肌张力受非肾上腺素能和非胆碱能神经递质的影响，并且通过生化研究已证实这些组织中存在功能性α1和α2肾上腺素能受体。这些变化受阴道和阴蒂中血管和非血管平滑肌张力的调节。原代细胞培养研究表明，几种生理调节剂，如血管活性肠肽（VIP）、一氧化氮（NO）和前列腺素E（PGE），可调节阴道平滑肌收缩。来自实验模型的数据对女性性唤起反应的机制提供了初步认识。
