The mammalian kidney consumes ATP at high rates for various transporti
ng processes. Renal tubular epithelial cells represent oxidative ATP s
ynthesis where the individual nephron segments have the preferred subs
trates. Measurement of ATP content is useful for assessing the target
site and intensity of nephrotic agents. Confocal microscopy has made m
ore precise analysis of structural alterations related to ATP depletio
n in renal tubular cells. Molecular cloning of P-2 purinoceptors is no
w giving a clear explanation of ATP's action in the kidney. ATP metabo
lism and P-2 purinoceptors, reviewed in this article, may provide a be
tter understanding of renal physiology and pathophysiology at the beds
ide.