Accompanying the subjective excitement and erotic feelings of arousal are a number of physical changes. These changes include genital swelling; increased vaginal lubrication; engorgement of the breasts and nipple erection; increases in skin sensitivity to sexual stimulation; changes in heart rate, blood pressure, muscle tone, breathing, body temperature; mottling of the skin; and a “sex ﬂush” of vasodilatation over the chest, breasts, and face.
With sexual stimulation, brain activity in the hypothalamus and other areas inﬂuencing the genital response are activated, triggering the autonomic nervous system to allow increased blood ﬂow to the vagina. Vasodilatation of the arterioles in the submucosal vaginal plexus increases transudation of interstitial ﬂuid, which moves from capillaries between the epithelial intercellular spaces and into the vaginal lumen. Simultaneously, the autonomic nervous system allows relaxation of the smooth muscle cells surrounding blood spaces (sinusoids) in the extensive clitoral tissue and labia, causing clitoral swelling and vasodilatation in the labia. Recent immunohistologic studies indicate nerves containing nitric oxide are present in the genital skin covering the clitoris and labia (5).
With arousal, the vagina lengthens, distends, and dilates, and the uterus elevates out of the pelvis. With increased sexual stimulation, vasocongestion reaches a maximum intensity.
Genitally, the labia become more swollen and darker red and the lower third of the vagina swells and thickens to form an “orgasmic platform.” The clitoris becomes more swollen and elevates to a position near the symphysis pubis, and the uterus elevates fully out of the pelvis. The breasts become more engorged, the skin more mottled, and the nipples more erect.
The neurobiology of arousal is incompletely understood but the genital vasocongestive responses appear to be highly automated, occurring within seconds of an erotic stimulus (23). Parasympathetic nerves release nitric oxide and vasoactive intestinal polypeptide (VIP), mediating vasodilatation (24,25). Acetylcholine (ACh) blocks noradrenergic vasoconstrictive mechanisms and promotes nitric oxide release from endothelium. The parasympathetic and sympathetic nervous systems and the somatic system function less independently than was previously believed. Communication was identified between the cavernous nerves to the clitoris, containing nitric oxide, and the distal portion of the (somatic) dorsal nerve of the clitoris from the pudendal nerve (5). The pelvic sympathetic nerves primarily release (vasoconstrictive) noradrenaline and adenosine triphosphate, but some release ACh, nitric oxide, and VIP. Nitric oxide is thought to be the major neurotransmitter involved in vulvar engorgement (5,25). In the vagina, VIP, nitric oxide, and other unidentified neurotransmitters are involved (25).