Renin-angiotensin-aldosterone system and the aging kidney

Abstract

Human senescence induces changes in the renin-angiotensin-aldosterone system (RAAS) which consists of a substantial decrease in its plasma activity. Consequently, the distal tubulés capability of handling sodium and potassium is significantly reduced in the elderly, while distal tubule acidification is slightly delayed but preserved in this age group. Several studies in animal models support the hypothesis that senile renal structural changes could be induced by the local production of angiotensin II, and also that enalapril significantly decreases senile mesangial expansion, glomerulosclerosis and peritubular and medullar interstitial sclerosis. The same applies to several highly prevalent diseases in the elderly, such as hypertension, obesity, cardiac insufficiency, chronic nephropathy and dementia. In conclusion, the relationship between the RAAS and senescence is complex, since not only does aging cause many changes on this hormonal system, but also RAAS overactivity seems to be one of the main inducing mechanisms for normal senescence, and for many prevalent diseases in the elderly.