PARATHYROID-HORMONE STIMULATES ELECTROGENIC SODIUM-TRANSPORT IN A6 CELLS

The effects of parathyroid hormone (PTH) on sodium homeostasis in the distal tubule are not well defined. Using A6 cells as a model for dist al tubular epithelium we measured equivalent short circuit current (le q), as an estimate of net sodium transport. We found that PTH increase d leq in a dose-dependent manner. DDA, an agent which inhibits adenyla te cyclase, decreased PTH-activated sodium transport, suggesting a rol e for cAMP elevation in PTH effects. Moreover, addition of Rp-cAMP, an inhibitor of cAMP-dependent protein kinase, partially blocked the PTH -stimulated leq. PTH also elicited a sustained increase in [Ca2+](i) i n A6 cells. This elevation in [Ca2+](i) was abolished by removal of ca lcium from the extracellular medium, suggesting the involvement of cal cium influx pathways. In fact, addition of the calcium channel blocker nitrendipine to PTH-stimulated leq partially blocked PTH-activated so dium transport. Taken together these data demonstrate that PTH stimula tes electrogenic sodium transport in A(6) cells and that this effect m ay be mediated through a rise in both intracellular calcium and cellul ar cAMP. (C) 1995 Academic Press, Inc.