Regulation of net bicarbonate transport in rabbit cortical collecting tubule by peritubular pH, carbon dioxide tension, and bicarbonate concentration.

Abstract

The effects of changes in peritubular pH, carbon dioxide tension (Pco2), and HCO3 concentration on net HCO3 transport was examined in in vitro perfused cortical collecting tubules (CCTs) from unpretreated New Zealand white rabbits. Lowering peritubular HCO3 concentration and pH by reciprocal replacement of HCO3 with Cl-, significantly stimulated net HCO3 absorption. Lowering peritubular HCO3 concentration and pH, by substitution of HCO3 with gluconate, while keeping Cl-concentration constant, also stimulated net HCO3 absorption. Raising peritubular HCO3 concentration and pH, by reciprocal replacement of Cl-with HCO3, inhibited net HCO3 absorption (or stimulated net HCO3 secretion). When the tubule was cooled, raising peritubular HCO3 concentration had no effect on net HCO3 transport, suggesting these results are not due to the passive flux of HCO3 down its concentration gradient.The effect of changes in ambient Pco2 on net HCO3 transport were also studied. Increasing the ambient Pco2 from 40 mmHg to either 80 or 120 mmHg, allowing pH to fall, had no effect on net HCO3 transport. Similarly, lowering ambient Pco2 to 14 mmHg had no effect on net HCO3 transport. Simultaneously increasing peritubular HCO3 concentration and Pco2, without accompanying changes in peritubular pH, i.e., isohydric changes, stimulated net HCO3 secretion to the same degree as nonisohydric increases in peritubular HCO3 concentration. Likewise, isohydric lowering of peritubular HCO3 concentration and Pco2 stimulated net HCO3 absorption.We conclude that: (a) acute changes in peritubular HCO3 concentration regulate acidification in the CCI and these effects are mediated by a transcellular process; (b) acute changes in ambient Pco2 within the physiologic range have no effect on HCO3 transport in the in vitro perfused CCI; and (c) acute in vitro regulation of CCI acidification is independent of peritubular pH.

Endogenous endothelins mediate increased distal tubule acidification induced by dietary acid in rats.

“…Dietary acid-induced alterations in body fluid acid- base parameters might increase distal nephron acidification directly. Although changes in environmental acid-base parameters can induce predictable alterations in acidification of renal epithelia studied in vitro (32,33), it is clear that sustained changes in plasma (3,24) or intracellular (4) acid-base parameters are not necessary to maintain altered renal epithelial acidification (3,4,24). Alternative or additional mechanisms include diet-induced modification of the level and/or activity of secretory substances that modify renal epithelial acidification.…”

Prostaglandin E2 inhibits sodium transport in rabbit cortical collecting duct by increasing intracellular calcium.

“…In vitro microperfusion of isolated cortical collecting ducts was performed as previously described (11). Briefly, rabbits weighing 1.5-2.5 kg were killed by using an intramuscular injection of ketamine (44 mg/kg) and xylazine (11 mg/kg) for anesthesia followed by decapitation.…”

Epidermal growth factor inhibits the hydroosmotic effect of vasopressin in the isolated perfused rabbit cortical collecting tubule.

“…After isolation, the CCT was transferred to a thermostatically controlled, flowing bath chamber, cannulated, and perfused with an isotonic solution as previously described (15). An isotonic bath solution was also used and bath flow Was adjusted to 0.5 ml/min using a perfusion pump (Sage Instruments, Inc., Cleveland, OH).…”