Abstract
Increasing evidence suggests that the ATP/P2 receptor system acts in an autocrine or paracrine fashion to affect various aspects of renal function. P2 receptors have been identified in most renal vessels and nephron segments; ATP is released from renal epithelial cells; and enzymes responsible for ATP breakdown are expressed in the vasculature and tubules. Stimulation of P2 receptors in the afferent arterioles by ATP released from renal nerve endings or from adjacent macula densa cells induces vasoconstriction and contributes to the control of renal haemodynamics. In the tubule, there is evidence for a variety of P2-mediated effects: inhibition of proximal tubular reabsorption; inhibition of Na + ,K + ,2Cl − cotransporter activity (through increased nitric oxide synthesis) in the thick ascending limb of the loop of Henle; inhibition of magnesium reabsorption in the distal tubule; and modulation of sodium and water reabsorption in the collecting duct. Finally, P2 receptors, particularly P2X subunits, appear to play an important role in renal pathology, specifically in cyst formation in polycystic kidney disease and in some forms of renal injury and inflammation.
Published Version
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