
Purpose of reviewAngiotensin II is a main regulator of kidney function. Renal actions mediated by the angiotensin AT(1) receptor have been well known for many years. In contrast, several details of angiotensin AT(2) receptor actions in kidney physiology and pathophysiology were only described very recently. These findings are reviewed in this article.Recent findingsRegarding the role of the angiotensin AT(2) receptor in kidney physiology, a major recent finding was that the AT(2) receptor-mediated inhibition of Na+-H+ exchanger-3 and Na+/K+-ATPase in the renal proximal tubules is caused by internalisation of these transporters, thus reducing reabsorption and increasing natriuresis/diuresis. Regarding renal pathology, several studies demonstrated an attenuation of renal injury caused by diabetes or by obesity with or without high-salt diet through anti-inflammatory, antifibrotic, and antioxidative mechanisms. Generally, AT(2) receptor expression seems increased and AT(2) receptor-mediated effects stronger in female and obese animals.SummaryThe recent findings about the role of the angiotensin AT(2) receptor in renal health and disease strongly suggest that pharmacological targeting of this receptor with selective agonists is a promising therapeutic strategy for inducing diuresis/natriuresis (also additive to established diuretics) and for the treatment of diabetic nephropathy or kidney disease of other pathogenesis.
RENAL-FUNCTION, BLOOD-PRESSURE, AT(2) RECEPTOR, angiotensin, renal physiology, II RECEPTORS, OBESE ZUCKER RATS, DIABETIC-NEPHROPATHY, FACTOR-KAPPA-B, AT2-receptor, AT2 RECEPTOR, nephropathy, COMPOUND 21, SPONTANEOUSLY HYPERTENSIVE-RATS
RENAL-FUNCTION, BLOOD-PRESSURE, AT(2) RECEPTOR, angiotensin, renal physiology, II RECEPTORS, OBESE ZUCKER RATS, DIABETIC-NEPHROPATHY, FACTOR-KAPPA-B, AT2-receptor, AT2 RECEPTOR, nephropathy, COMPOUND 21, SPONTANEOUSLY HYPERTENSIVE-RATS
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