Augusta, GA) In human diabetic patients, an excessive vasoconstrictive and pro-aggregatory thromboxane (TXA2) renal synthesis, along with a decrease in vasodilatory and anti-aggregatory prostaglandin (PGE2) synthesis, has been found to influence kidney function. Prostaglandins and thromboxane are formed by the enzymatic oxidation of arachidonic acid catalyzed by the cyclooxygenases, COX 1 and COX-2. Recently developed non-steroidal anti-inflammatory drugs (NSAIDS) are targeted to inhibit COX-2 and treat inflammation and arthritic pain. It is not known if the use of NSAIDS may be beneficial for the treatment of kidney disease; however, the upregulation of pro-inflammatory COX-2 and increased production of COX-2 derived metabolites have been implicated in diabetic nephropathy. COX-2 regulation and its association with renal damage are not known in the Obese Zucker rat. A new study tests the hypothesis that altered kidney regulation of COX-2 occurs at a very early stage in the progression of kidney disease.
A New Study
The authors of the study entitled, "Renal Microvascular COX-2 Upregulation is Associated with Kidney Damage in Zucker Obese Rats," are Aparajita Dey, Roger S. Williams, David M. Pollock, David W. Stepp and John D. Imig, all from the Vascular Biology Center, Medical College of Georgia, Augusta, GA. They are presenting their findings during the American Physiological Society (APS) (www.the-aps.org) conference, Understanding Renal and Cardiovascular Function Through Physiological Genomics. The scientific conference is being held October 1-4, 2003 at the Radisson Riverfront Hotel and Convention Center, Augusta, GA.
Background
Obesity, a major nutritional disorder in the United States, leads to the development of Type II diabetes, hypertension, atherosclerosis and chronic renal disease, most of which are interdependent factors. Diabetic nephropathy, a kidney disease that devel
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Contact: Donna Krupa
djkrupa1@aol.com
703-527-7357
American Physiological Society
30-Sep-2003
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