Chronic DOC treatment enhances Na(+)-H+ exchanger activity of beta-intercalated cells in rabbit CCD.

Chronic deoxycorticosterone (DOC) treatment is known to increase HCO3- secretion in rabbit cortical collecting ducts (CCD). In this study, we examined whether changes in number or function of intercalated cells (ICC) are induced by DOC treatment. The number of total ICC [acetoxymethyl ester of 2',7'-bis(2-carboxyethyl)-5(6)-carboxyfluorescein (BCECF/AM)-positive cells after its luminal loading], and beta-ICC (peanut agglutinin-positive cells) was not different between DOC and control groups in either initial CCD or terminal CCD. To evaluate the single-cell function of ICC, the rate of intracellular pH (pHi) recovery (dpHi/dt, pHU/s x 10(3)) after NH4+/NH3 prepulse was studied in the in vitro microperfused CCD in the presence of HCO3-/CO2 with BCECF/AM. The mean rate of dpHi/dt of beta-ICC in the DOC group was faster than that in the control group (6.19 +/- 0.36 vs. 4.30 +/- 0.41, P less than 0.005, respectively), whereas baseline pHi and buffer capacity were similar in the two groups. The inhibition of basolateral Na(+)-H+ exchanger with 1 mM amiloride eliminated the difference of dpHi/dt between the two groups, indicating the increased activity of basolateral Na(+)-H+ exchanger of beta-ICC in the DOC group. The correction of DOC-induced metabolic alkalosis by oral acid loading abolished the increase in Na+/H+ exchanger activity by chronic DOC treatment. These results suggest that DOC treatment induces a functional change in a single beta-ICC and that this functional change was induced by in vivo acid-base status.