The first phase of the female sexual response, associated with neurotransmitter-mediated vascular smooth muscle relaxation, results in increased vaginal lubrication, wall engorgement and luminal diameter as well as increased clitoral length and diameter. Specific physiologic impairments of vasculogenic female sexual dysfunction include vaginal engorgement and clitoral erectile insufficiency syndromes. These syndromes exist when during sexual stimulation abnormal arterial circulation into the vagina or clitoris, usually from atherosclerotic vascular disease, interferes with normal vascular physiologic processes. Clinical symptoms may include delayed vaginal engorgement, diminished vaginal lubrication, pain or discomfort with intercourse, diminished vaginal sensation, diminished vaginal orgasm, diminished clitoral sensation or diminished clitoral orgasm. An animal model of this syndrome, with significant physiologic responses between the control and the atherosclerotic pelvic nerve stimulated hemodynamic responses, is discussed. Non-atherosclerotic, traumatic vascular disease of the ilio-hypogastric-pudendal arterial bed from pelvic fractures or blunt perineal trauma may also result in diminished vaginal/clitoral arterial blood flow following sexual stimulation. Diagnostic studies assessing the hemodynamic integrity of the ilio-hypogastric-pudendal arterial bed to the vagina and clitoris and new oral/topical pharmacologic strategies for enhancing vaginal/clitoral blood flow in patients with vasculogenic female sexual dysfunction are discussed. There is a growing body of evidence that women with sexual dysfunction will commonly have physiologic abnormalities, such as vasculogenic female sexual dysfunction, contributing to their overall sexual health problems.