One needs only turn on the television to understand that significant advances have been made in the cure and treatment of male sexual dysfunction. Less visible progress has been made in understanding and treating female sexual disorders (FSD), a complex and multi-layered problem.
A team of researchers has undertaken a new approach in the lab to understanding how and why FSD occurs in general, and the impact of the vasculature (the vessels in the body that carry blood, such as arteries and veins) in particular. The findings of their latest study suggest that the drugs that help men may some day also address some forms of female sexual dysfunction.
The study, Phosphodiesterase Type 5 Inhibitors Relax Female Rat Internal Pudendal Arteries: Potential Treatment for Female Sexual Dysfunction, was conducted by Kyan J. Allahdadi, Rita C. Tostes, and R. Clinton Webb, all of the Medical College of Georgia, Augusta, GA. Dr. Allahdadi and his colleagues are presenting their findings at the 122nd Annual Meeting of the American Physiological Society, which is part of the Experimental Biology 2009 scientific conference. The meeting will be held April 18-22, 2009 in New Orleans.
New evidence suggests that female sexual dysfunction may be, in part, the result of inadequate supply of blood to the female genitals and may be addressed with erectile dysfunction drugs. Originally developed as therapy for hypertension, these drugs work by dilating blood vessels sufficiently to produce erections in males. These drugs have not been fully explored in females.
The researchers used an animal model and compared the effects of three drugs used for erectile dysfunction (the phosphodiesterase 5 inhibitors (PDE5I, such as Viagra® (sildenafil); Levitra® (vardenafil); and Cialis® (tadalafil)). PDE5I was used and analyzed in female and male rat internal pudendal arteries. The internal pudendal artery supplies blood to the penis in men and to the vagina and clitoris in women. Arterial segments were contracted with phenylephrine then submitted to increasing concentrations of one of the PDE5 inhibitors.
The internal pudendal arteries of both male and female rats (n=10 to12) were measured for constriction/dilation.
The researchers found the following:
Percent maximum relaxation (Top), effective concentration to relax 50% (Bottom)
Female Arteries Concentration/Dependency: 105.00±7.73; 6.60±1.7
Male Arteries Concentration/Dependency: 103±0.9; 5.67±0.9
Female Arteries Concentration/Dependency: 115.6±11.63; 6.67±0.24
Male Arteries Concentration/Dependency: 105.1±89.88; 6.4±0.23
Female Arteries Concentration/Dependency: 80.13±5.39; 7.98±0.24
Male Arteries Concentration/Dependency: 102.3±23.65; 5.4±0.23
· All the PDE5I inhibitors relaxed both female and male rat internal pudendal arteries, indicating that these arteries from both female and male rats are sensitive to PDE5I. However, female internal pudendal arteries were more sensitive to sildenafil at a lower concentration, which suggests it may be effective at a lower dose than vardenafil.
· Male internal pudendal arteries reacted more effectively to vardenafil. Female internal pudendal arteries also reacted differently in comparison to the male arteries in that they demonstrated an oscillatory behavior by both dilating and contracting, suggesting that PDE5I may have a different mechanism of action in females.
According to Dr. Allahdadi, "PDE5I may be useful in the treatment of female sexual dysfunction caused by inadequate blood supply through the internal pudendal artery. The significant difference in how male and female pudendal arteries react to PDE5 inhibitors merits further study."
The study team is currently exploring the different relaxation profile observed between female and male rat internal pudendal arteries as well as functional abnormalities in internal pudendal arteries from diabetic rats.
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