Calcitonin stimulates H+ secretion in rat kidney intercalated cells

Calcitonin (CT) modulates rat intercalated cell. (IC) functions of the rat cortical collecting duct (CCD) [E. Siga, B. Mandon, N. Roinel, and C. de Rouffignac. Am.J. Physiol. 264 (Renal Fluid Electrolyte Physiol. 33): F221-F227, 1993]. To characterize the specific function regulated by CT, rat CCDs were perfused in vitro. Total CO2 net fluxes (J(tCO2), pmol . mm(-1). min(-1)) and transepithelial voltage (Vt) were measured. Bath CT induced a significant tCO(2) reabsorption. This effect was higher on CCDs harvested from acid-loaded than from control rats. When HCO3- secretion was blocked, CT also raised J(tCO2) and V-t. When H+ secretion was blocked, CT was ineffective on J(tCO2) and V-t. When HCO3- secretion was increased and H+ secretion was inhibited, CT did not change J(tCO2), whereas isoproterenol (ISO) increased tCO(2) secretion from -13.5 +/- 2.0 (control) to -19.0 +/- 2.4 (ISO). In rat CCD studied under these same preceding conditions plus luminal amiloride to block the Na+-dependent V-t, CT did not alter V-t, whereas ISO increased it by 4.5 +/- 0.7 mV. We conclude from these data that, in the rat CCD, calcitonin stimulates H+ secretion, likely by so-called alpha-intercalated (alpha-IC) cells, whereas ISO stimulates HCO3- secretion, likely by so-called beta-IC cells.