Hemodynamic basis for the limited renal injury in rats with Angiotensin II-induced hypertension.

Hemodynamic basis for the limited renal injury in rats with Angiotensin II-induced hypertension. Am J Physiol Renal Physiol. 2014 Dec 4;:ajprenal.00596.2014 Authors: Polichnowski AJ, Griffin KA, Picken MM, Licea-Vargas H, Long J, Williamson GA, Bidani AK Abstract ANG II is thought to increase the susceptibility to hypertension-induced renal disease (HIRD) via BP-dependent and BP-independent pathways; however, the quantitative relationships between BP and HIRD have not been examined in ANG II-infused hypertensive rats. We compared the relationship between radiotelemetrically-measured BP and HIRD in Sprague-Dawley rats (Harlan) chronically administered ANG II (300-500 ng/kg/min, n=19) for 4 weeks vs. another commonly employed pharmacologic model of hypertension induced by the chronic administration of N(ω)-nitro-L-arginine methyl ester (L-NAME, 50 mg/kg/day, n=23). Despite the significantly higher average systolic BP associated with ANG II (191.1±3.2 mmHg) vs. L-NAME (179.9±2.5 mmHg) administration; the level of HIRD was very modest in the ANG II vs. L-NAME model as evidenced by significantly less glomerular injury (6.6±1.3% vs. 11.3±1.5, respectively), tubulointerstitial injury (0.3±0.1 vs. 0.7±0.1 injury score, respectively), proteinuria (66.3±10.0 mg/day vs. 117.5±10.1, respectively) and serum creatinine (0.5±0.04 mg/dl vs. 0.9±0.07, respectively). Given that HIRD severity is expected to be a function of renal microvascul...
Source: Am J Physiol Renal P... - Category: Urology & Nephrology Authors: Tags: Am J Physiol Renal Physiol Source Type: research