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.
The researchers examined the erectile response (ICP/MAP) to pelvic ganglion stimulation using lean and obese-d
Contact: Donna Krupa
American Physiological Society