Prostacyclin increases distal tubule HCO3 secretion in the rat

We examined whether prostacyclin (PGI(2)), a prostaglandin synthesized in the renal cortex that increases adenosine 3',5'-cyclic monophosphate levels in distal nephron epithelia, mediates increased HCO3 secretion in in vivo perfused distal tubules of anesthetized rats given dietary HCO3. Animals eating a minimum electrolyte diet given 80 mM NaHCO3 drinking solution increased urine excretion of 6-keto-PGF(1 alpha), a PGI(2) metabolite, by 2.6 +/- 0.3-fold compared with those drinking distilled H2O. NaHCO3 animals infused with indomethacin to inhibit PGI(2) synthesis had lower HCO3 secretion than those without indomethacin (-8.9 +/- 0.9 vs. -18.7 +/- 1.8 pmol . mm(-1). min(-1), P < 0.01). By contrast, NaHCO3 animals infused with both PGI(2) and indomethacin had higher HCO3 secretion than those given indomethacin alone (-16.0 +/- 1.5, P < 0.02 vs. indomethacin group). HCO3 secretion was not different between controls with and without indomethacin but was higher in the PGI(2) + indomethacin compared with the indomethacin alone controls (-11.2 +/- 1.2 vs. -4.5 +/- 0.5, P < 0.01). The data show that PGI(2) increases distal tubule HCO3 secretion in rats and suggest that this agent contributes to the increased distal tubule HCO3 secretion induced by dietary HCO3.