Munarriz Ricardo, Kim Soo Wong, Kim Noel N, Traish Abdulmaged, Goldstein Irwin
Institute for Sexual Medicine, Department of Urology, Boston University School of Medicine, 720 Harrison Ave., Suite 600, Boston, Massachusetts 02118, USA.
J Urol. 2003 Aug;170(2 Pt 2):S40-4; discussion S44-5. doi: 10.1097/01.ju.0000075352.03144.15.
We review contemporary scientific data concerning the physiology and pharmacology of peripheral female genital arousal responses in the animal (rabbit and rat) model.
We reviewed the contemporary literature and our research studies concerning physiology and pharmacology of peripheral genital arousal from 3 experimental animal models, including genital smooth muscle cell culture, genital strip organ bath and in vivo animal model studies.
Nitric oxide (NO) appears to be a key pathway mediating clitoral smooth muscle relaxation. In the vagina NO appeared to have a more controversial role in mediating vaginal muscularis smooth muscle relaxation. Vasoactive intestinal polypeptide induced vaginal smooth muscle relaxation. Functional alpha-adrenergic receptors were expressed in the clitoris and vagina, and mediated norepinephrine induced genital smooth muscle contraction. Androgens and estrogens modulated distinct physiological responses in vagina, and androgens facilitated vaginal smooth muscle relaxation. Papaverine hydrochloride, a smooth muscle relaxant, and phentolamine mesylate, an alpha-blocker, administered into the vaginal spongy muscularis layer increased vaginal wall pressure and vaginal blood flow. Sildenafil caused significant increases in genital (clitoral and vaginal) blood flow and vaginal lubrication in intact and ovariectomized animals. This response was more pronounced in animals treated with estradiol, suggesting that the NO cyclic guanosine monophosphate pathway is involved in the physiological mechanism of female genital arousal and that sildenafil facilitates this response in an in vivo animal model.
To achieve improved understanding of the biological aspects of female sexual function, further research is needed in the physiology and pharmacology of peripheral (clitoral and vaginal) genital arousal in the animal model.
我们回顾了有关动物(兔和大鼠)模型中外周女性生殖器唤起反应的生理学和药理学的当代科学数据。
我们回顾了当代文献以及我们关于3种实验动物模型中外周生殖器唤起的生理学和药理学的研究,包括生殖器平滑肌细胞培养、生殖器条离体器官浴和体内动物模型研究。
一氧化氮(NO)似乎是介导阴蒂平滑肌松弛的关键途径。在阴道中,NO在介导阴道肌层平滑肌松弛方面的作用似乎更具争议性。血管活性肠肽可诱导阴道平滑肌松弛。功能性α-肾上腺素能受体在阴蒂和阴道中表达,并介导去甲肾上腺素诱导的生殖器平滑肌收缩。雄激素和雌激素调节阴道中不同的生理反应,雄激素促进阴道平滑肌松弛。将平滑肌松弛剂盐酸罂粟碱和α受体阻滞剂甲磺酸酚妥拉明注入阴道海绵肌层可增加阴道壁压力和阴道血流量。西地那非可使完整和去卵巢动物的生殖器(阴蒂和阴道)血流量及阴道润滑显著增加。在用雌二醇治疗的动物中这种反应更明显,表明NO-环磷酸鸟苷途径参与女性生殖器唤起的生理机制,并且西地那非在体内动物模型中促进了这种反应。
为了更好地理解女性性功能的生物学方面,需要对动物模型中外周(阴蒂和阴道)生殖器唤起的生理学和药理学进行进一步研究。