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Could a specific protein contribute to erectile dysfunction for the diabetic and obese?

(Augusta, GA) More than eight million men are at risk for erectile dysfunction (ED) induced by Type II (insulin resistant) diabetes. While the exact mechanism(s) involved in diabetes mellitus induced erectile dysfunction (DMED) is not yet understood, a team of researchers has hypothesized that certain proteins may regulate penile vascular tone increasing sensitivity to the action of vasoconstrictor agents. Their findings suggest that protein kinase C (PKC) may contribute to an enhanced vasoconstriction of the penile circulation and reduced erectile response.

Constriction of the penile vasculature prevents erection and is largely mediated by two agents: -adrenergic agonists or endothelin (ET-1). These agents cause vasoconstriction by activating phospholipase C (PLC) and result in the generation of inositol triphosphate (IP3) and diacylglycerol (DAG). This pathway is believed to recruit PKC in the constrictor response. Researchers have tested the hypothesis that in diabetic-obese Zucker rats, there is a depressed erectile response caused by increased action of the vasoconstrictor pathway involving PKC in a key sensitization process.

A New Study

The authors of a new study entitled "Altered Penile Vascular Reactivity and Erection of the Zucker Rat: A Role for PKC Ca2+ Sensitization," are Christopher J. Wingard, Delores Young, Katherine Lane and Shadhid Husain, all of the Department of Physiology, the Medical College of Georgia, Augusta, GA. They will present their findings during the upcoming scientific conference, Understanding Renal and Cardiovascular Function Through Physiological Genomics, a meeting of the American Physiological Society (APS) (www.the-aps.org), being held October 1-4, 2003 at the Radisson Riverfront Hotel and Convention Center, Augusta, GA.

Methodology

The researchers examined the erectile response (ICP/MAP) to pelvic ganglion stimulation using lean and obese-d
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Contact: Donna Krupa
djkrupa1@aol.com
703-527-7357
American Physiological Society
30-Sep-2003


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