Urinary calcium excretion is regulated homeostatically. Regulation is achieved, in part, by the action of parathyroid hormone on Ca2+absorption in the distal nephron. Parathyroid hormone increases Ca2+absorption in the cortical portion of the thick ascending limb of Henle's loop in all species studied, in the murine distal convoluted tubule, and in the rabbit connecting tubule. All of these sites contain parathyroid hormone-stimulated adenylate cyclase. Both cellular and paracellular pathways of Ca2+absorption are regulated by parathyroid hormone in the cortical portion of the thick ascending limb of Henle's loop. In both distal convoluted and connecting tubule cells, parathyroid hormone regulates transcellular Ca2+absorption by controlling the insertion and open probability of luminal plasmalemmal Ca2+ion channels. These channels are stimulated and inhibited by L-type calcium channel agonists and antagonists, repectively, but differ from similar channels in excitable cells in that membrane depolarization does not activate them. Parathyroid hormone also increases the driving force for diffusional Ca2+ion entry from the luminal fluid into the cytosol by increasing the intracellular negative electrical potential (at least in murine distal convoluted tubule cells) by increasing the chloride ion conductance of the basolateral cell membrane. The effects of parathyroid hormone on the other components of cellular Ca2+transport, via both protein kinases A and C and their interactions, remain to be examined.