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. Author manuscript; available in PMC: 2011 Feb 24.
Published in final edited form as: Curr Diab Rep. 2010 Aug;10(4):297–305. doi: 10.1007/s11892-010-0126-2

Fig. 1.

Fig. 1

Components of the renin-angiotensin-aldosterone system (RAAS), pathophysiologic actions of the RAAS, and pharmacologic agents clinically available to block the RAAS. Angiotensin (AT) II raises intraglomerular pressure through efferent arteriolar vasoconstriction, increases sodium reabsorption in the proximal tubule, and directly stimulates tubulointerstitial fibrosis. Aldosterone promotes distal renal sodium retention and stimulates tubulointerstitial fibrosis. ACEI—angiotensin-converting enzyme inhibitor; ARB—angiotensin receptor blocker; DRI— direct renin inhibitor