A review of the physiology and pharmacology of peripheral (vaginal and clitoral) female genital arousal in the animal model.

PURPOSE: We review contemporary scientific data concerning the physiology and pharmacology of peripheral female genital arousal responses in the animal (rabbit and rat) model.

MATERIALS AND

METHODS

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.

RESULTS

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.

CONCLUSIONS

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.