Chronic angiotensin II (Ang II) infusion for one or two weeks leads to progressive hypertension and induces inward hypertrophic remodeling in preglomerular vessels, which is associated with increased renal vascular resistance (RVR) and decreased glomerular perfusion. Considering the ability of preglomerular vessels to exhibit adaptive responses, the present study was performed to evaluate glomerular perfusion and renal function after six weeks of Ang II infusion. To address this study, male Wistar rats were submitted to fictitious surgery (control) or osmotic minipump insertion (Ang II 200 ng/kg/min, 42 days). A group of animals were treated or co-treated with losartan (10 mg/kg/day), an AT1 receptor antagonist, between the 28th and 42nd day. Chronic Ang II infusion increased systolic blood pressure to 185 ± 4 mmHg compared with 108 ± 2 mmHg in control rats. Concomitantly, Ang II-induced hypertension increased intrarenal Ang II level and consequently, preglomerular and glomerular injury. Under this condition, Ang II enhanced the total renal plasma flow (RPF), glomerular filtration rate (GFR), urine flow and induced pressure natriuresis. These changes were accompanied by lower RVR and enlargement of the lumen of interlobular arteries and afferent arterioles, consistent with impairment of renal autoregulatory capability and outward preglomerular remodeling. The glomerular injury culminated with podocyte effacement, albuminuria, tubulointerstitial macrophage infiltration and intrarenal extracellular matrix accumulation. Losartan attenuated most of the effects of Ang II. Our findings provide new information regarding the contribution of Ang II infusion over two weeks to renal hemodynamics and function via AT1 receptor.
- Angiotensin II
- renovascular remodeling
- Copyright © 2015, American Journal of Physiology - Renal Physiology