期刊
AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY
卷 278, 期 2, 页码 F219-F226出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajprenal.2000.278.2.F219
关键词
proton-potassium-exchanging ATPase; kidney tubules; collecting ducts; hydrogen ion concentration; proton-transporting ATP synthase; rabbits
资金
- NIDDK NIH HHS [DK-45788, DK-49750] Funding Source: Medline
Both acidosis and hypokalemia stimulate renal ammoniagenesis, and both regulate urinary proton and potassium excretion. We hypothesized that ammonia might play an important role in this processing by stimulating H+-K+-ATPase-mediated ion transport. Rabbit cortical collecting ducts (CCD) were studied using in vitro microperfusion, bicarbonate reabsorption was measured using microcalorimetry, and intracellular pH (pH(i)) was measured using the fluorescent, pH-sensitive dye, 2',7'-bis(2-carboxyethyl)-5(6)-carboxyfluorescein (BCECF). Ammonia caused a concentration-dependent increase in net bicarbonate reabsorption that was inhibited by luminal addition of either of the H+-K+-ATPase inhibitors, Sch-28080 or ouabain. The stimulation of net bicarbonate reabsorption was not mediated through apical H+-ATPase, basolateral Na+-K+-ATPase, or luminal electronegativity. Although ammonia caused intracellular acidification, similar changes in pHi induced by inhibiting basolateral Na+/H+ exchange did not alter net bicarbonate reabsorption. We conclude that ammonia regulates CCD proton and potassium transport, at least in part, by stimulating apical H+-K+-ATPase.
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