Biochemical factors modulating female genital sexual arousal physiology.
BACKGROUND
Female genital sexual arousal responses are complex neurophysiological processes consisting of central and peripheral components that occur following sexual stimulation. The peripheral responses in sexual arousal include genital vasocongestion, engorgement and lubrication resulting from a surge of vaginal and clitoral blood flow. These hemodynamic events are mediated by a host of neurotransmitters and vasoactive agents.


OBJECTIVE
To discuss the role of various biochemical factors modulating female genital sexual arousal responses.


METHODS
A comprehensive literature review was conducted using the PubMed database and citations were selected, based on topical relevance, and examined for study methodology and major findings.


METHODS
Data from peer-reviewed publications.


RESULTS
Adrenergic as well as non-adrenergic non-cholinergic neurotransmitters play an important role in regulating genital physiological responses by mediating vascular and non-vascular smooth muscle contractility. Vasoactive peptides and neuropeptides also modulate genital sexual responses by regulating vascular and non-vascular smooth muscle cells and epithelial function. The endocrine milieu, particularly sex steroid hormones, is critical in the maintenance of tissue structure and function. Reduced levels of estrogens and androgen are associated with dramatic alterations in genital tissue structure, including the nerve network, as well as the response to physiological modulators. Furthermore, estrogen and androgen deficiency is associated with reduced expression of sex steroid receptors and most importantly with attenuated genital blood flow and lubrication in response to pelvic nerve stimulation.


CONCLUSIONS
This article provides an integrated framework describing the physiological and molecular basis of various pathophysiological conditions associated with female genital sexual arousal dysfunction.
Traish
Abdulmaged M
AM
Boston University School of Medicine, Department of Biochemistry, Boston, MA 02118, USA. atraish@bu.edu
Botchevar
Ella
E
Kim
Noel N
NN
D000818:Animals; D000928:Antidepressive Agents / Q000009:adverse effects; D001143:Arousal / Q000502:physiology*; D050197:Atherosclerosis / Q000503:physiopathology; D002582:Cervix Mucus / Q000502:physiology; D002987:Clitoris / Q000378:metabolism / Q000502:physiology; D003920:Diabetes Mellitus / Q000503:physiopathology; D004958:Estradiol / Q000378:metabolism; D005260:Female; D006801:Humans; D009119:Muscle Contraction / Q000502:physiology; D009129:Muscle Tonus / Q000502:physiology; D018482:Muscle, Skeletal / Q000378:metabolism / Q000502:physiology; D009130:Muscle, Smooth / Q000378:metabolism / Q000502:physiology; D009479:Neuropeptides / Q000378:metabolism; D018377:Neurotransmitter Agents / Q000378:metabolism; D011944:Receptors, Androgen / Q000378:metabolism; D011960:Receptors, Estrogen / Q000378:metabolism; D011983:Receptors, Purinergic / Q000378:metabolism; D012039:Regional Blood Flow / Q000502:physiology; D012735:Sexual Dysfunction, Physiological / Q000503:physiopathology; D013739:Testosterone / Q000378:metabolism; D014621:Vagina / Q000098:blood supply / Q000294:innervation / Q000378:metabolism / Q000502:physiology*
D000928:Antidepressive Agents; D009479:Neuropeptides; D018377:Neurotransmitter Agents; D011944:Receptors, Androgen; D011960:Receptors, Estrogen; D011983:Receptors, Purinergic; D013739:Testosterone; D004958:Estradiol