Effects of ammonia on acid-base transport by the B-Type intercalated cell

Ammonia, in addition to its role as a constituent of urinary net acid excre tion, stimulates cortical collecting duct (CCD) net bicarbonate reabsorptio n. The current study sought to begin determining the cellular transport pro cesses through which ammonia regulates bicarbonate reabsorption by testing whether ammonia stimulates B-type intercalated cell bicarbonate secretion, bicarbonate reabsorption, or both. The effects of ammonia on single CCD int ercalated cells was studied by use of measurements of intracellular pH take n from in vitro microperfused CCD segments after luminal loading of the pH- sensitive fluorescent dye BCECF. These results showed, first, that ammonia inhibited B-cell unidirectional bicarbonate secretion and that this occurre d despite no effect of ammonia on apical Cl-/HCO3- exchange activity. Secon d, ammonia increased the contribution of a SCH28080-sensitive apical H+-K+- ATPase to basal intracellular pH regulation and it stimulated basolateral C l-/HCO3- exchange activity. Thus, ammonia activated both apical proton secr etion and basolateral base exit, consistent with stimulation of unidirectio nal bicarbonate reabsorption. It was concluded that ammonia regulates CCD n et bicarbonate reabsorption, at least in part, through the coordinated regu lation of the separate processes of B-cell bicarbonate reabsorption and bic arbonate secretion. These effects do not reflect a general activation of io n transport but, instead, reflect coordinated and specific regulation of io n transport.