Reckelhoff J F, Zhang H, Srivastava K, Roberts L J, Morrow J D, Romero J C
Department of Physiology and Biophysics and The Center for Excellence for Cardiovascular-Renal Research, University of Mississippi Medical Center, Jackson 39216-4505, USA.
Hypertension. 2000 Jan;35(1 Pt 2):476-9. doi: 10.1161/01.hyp.35.1.476.
The present study was performed to determine whether physiologically relevant doses of angiotensin II (Ang II), which do not affect renal hemodynamics but do cause slow response hypertension, result in oxidative stress as measured by production of vasoconstrictor F(2)-isoprostane, a prostaglandin-like non-cyclooxygenase-produced arachidonic acid metabolite that is the end product of lipid peroxidation. Rats were instrumented with abdominal aortic and left femoral venous catheters, and before and throughout Ang II (or saline) infusion, all rats received enalapril (250 mg/L). Four days after the initiation of enalapril, rats were infused with Ang II (10 ng. kg(-1). min(-1), n=6) or saline (n=6) for 14 days. Mean arterial pressure was measured 24 hours per day, and on day 12, glomerular filtration rate and renal plasma flow were measured. Mean arterial pressure in control rats averaged 85+/-1 mm Hg, and with Ang II infusion, mean arterial pressure increased slowly and reached a plateau on day 3, averaging 117+/-2 mm Hg (P<0.0001 compared with enalapril alone). Glomerular filtration rate and renal plasma flow were not affected by Ang II. Free F(2)-isoprostanes in plasma increased by 54% with Ang II (P<0.01), and the production of F(2)-isoprostanes esterified in plasma lipids tended to be higher with Ang II also but did not reach significance (P=0.1). These studies suggest that low doses of Ang II are capable of producing oxidative stress in animals. Whether oxidative stress plays a causative role in Ang II-mediated slow-response hypertension or is secondary to the hypertension is not clear from these data and will require further study.
