Genetic deletion of the angiotensin-(1-7) receptor Mas leads to glomerular hyperfiltration and microalbuminuria.

摘要: Angiotensin-(1–7), an active fragment of both angiotensins I and II, generally opposes the vascular proliferative actions angiotensin II. Here we evaluated effects angiotensin-(1–7) receptor Mas on renal physiology morphology using Mas-knockout mice. Compared to wild-type animals, knockout mice had significant reductions in urine volume fractional sodium excretion without any change free-water clearance. A significantly higher inulin clearance microalbuminuria concomitant with a reduced blood flow suggest that glomerular hyperfiltration occurs Histological analysis found tuft diameter increased expression collagen IV fibronectin mesangium interstitium, along III interstitium. These fibrogenic changes dysfunction were associated upregulation II AT1 transforming growth factor-β mRNA. Our study suggests acts as critical regulator fibrogenesis by controlling transduced through receptors kidney.