Journal
KIDNEY INTERNATIONAL
Volume 75, Issue 11, Pages 1184-1193Publisher
ELSEVIER SCIENCE INC
DOI: 10.1038/ki.2009.61
Keywords
angiotensin-(1-7); angiotensin II; AT(1) receptor; receptor Mas; renal fibrosis; transforming growth factor-beta
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Funding
- FAPEMIG ( Fundacao de Amparo a Pesquisa do Estado de Minas Gerais, Brazil)
- CNPq ( Conselho Nacional de Desenvolvimento Cientifico e Tecnologico, Brazil)
- PRONEX ( Programa de Grupos de Excelencia-FINEP, Brazil)
- DFG ( Deutsche Forschungsgemeinschaft, Germany)
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Angiotensin-(1-7), an active fragment of both angiotensins I and II, generally opposes the vascular and proliferative actions of angiotensin II. Here we evaluated effects of the angiotensin-(1-7) receptor Mas on renal physiology and morphology using Mas-knockout mice. Compared to the wild-type animals, Mas knockout mice had significant reductions in urine volume and fractional sodium excretion without any significant change in free-water clearance. A significantly higher inulin clearance and microalbuminuria concomitant with a reduced renal blood flow suggest that glomerular hyperfiltration occurs in the knockout mice. Histological analysis found reduced glomerular tuft diameter and increased expression of collagen IV and fibronectin in the both the mesangium and interstitium, along with increased collagen III in the interstitium. These fibrogenic changes and the renal dysfunction of the knockout mice were associated with an upregulation of angiotensin II AT1 receptor and transforming growth factor-beta mRNA. Our study suggests that Mas acts as a critical regulator of renal fibrogenesis by controlling effects transduced through angiotensin II AT1 receptors in the kidney. Kidney International (2009) 75, 1184-1193; doi:10.1038/ki. 2009.61; published online 4 March 2009
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