Purinoceptor regulation of renal tubular transport is coming of age.

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a central role in regulating blood pressure,body fluid volume, body fluid composition, and electrolyte andwater balance. Generations of effort have gone into under-standing the tubular and vascular interactions that confer in-credible fidelity in accomplishing these essential functions.While P2 purinergic signaling systems were investigated inother organ systems for some time, the role P2 receptors playin influencing renal vascular and tubular function did not reallybegin to develop until about 1990. Since then, investigatorshave provided considerable evidence that P2 receptors areinvolved in many aspects of renal vascular and tubular physi-ology. ATP is released by renal tissues (13, 14, 27) includingmacula densa (3, 10), loop of Henle (22, 24), cortical collectingduct (6), and probably proximal tubule (26). In each of thesetubular segments, physiologic control of renal transport mech-anisms is implicated, but the specific mechanisms by whichthat regulation occurs are not completely understood. Thecurrent report from Silva and Garvin (22a) now advances therole of ATP and P2 receptor activation in regulating tubularfunction in the thick ascending loop of Henle.Aside from the important roles P2 receptors play in regulat-ing microvascular autoregulatory function (5), P2 receptors arewidely expressed by tubular epithelial cells (19, 23, 25).Detection of ATP release by renal epithelial cells spurredinterest in the possibility that tubular transport function couldbe under purinergic control (11, 19, 25, 30). There is compel-lingevidencethatlocallyreleasedATPexertsautocrinecontrolof epithelial sodium channel (ENaC) activity in the apicalmembrane of mouse cortical collecting duct cells (16, 20, 25,29). Data indicate that ATP-dependent suppression of apicalENaC activity involves P2Y