31P-NMR in vivo measurement of renal intracellular pH: effects of acidosis and K+ depletion in rats
Adam, W.R.; Koretsky, A.P.; Weiner, M.W.
American Journal of Physiology 251(5 Pt 2): F904-F910
1986
ISSN/ISBN: 0002-9513 PMID: 3777186 Document Number: 276015
Renal intracellular pH (pHi) was estimated in vivo from the chemical shift ( sigma ) of inorganic phosphate (Pi), obtained by 31P-nuclear magnetic resonance spectroscopy (NMR). pH was calculated from the difference between sigma Pi and sigma alpha -ATP. Renal pH in control rats was 7.39 +or- 0.04. Rats were subjected to acute (less than 24 h) and chronic (4 to 7 days) metabolic acidosis, acute (20 min) and chronic (6 to 8 days) respiratory acidosis and dietary potassium depletion (7 to 21 days). Acute metabolic and respiratory acidosis produced acidification of renal pHi. Chronic metabolic acidosis (arterial blood pH, 7.26 +or- 0.02) lowered renal pHi to 7.30 +or- 0.02, but chronic respiratory acidosis (arterial blood pH, 7.30 +or- 0.05) was not associated with renal acidosis (pH, 7.40 +or- 0.04). At a similar blood pH, pHi was higher in chronic metabolic acidosis than in acute metabolic acidosis, suggesting an adaptive process that raises pHi. K depletion (arterial blood pH, 7.44 +or- 0.05) was associated with renal acidosis (renal pH, 7.17 +or- 0.02). There was a direct relation between renal pH and cardiac K+. Rapid partial repletion with KCl (1 mmol) significantly increased renal pHi from 7.14 +or- 0.03 to 7.31 +or- 0.01. The fall of renal pHi produced by acute metabolic and respiratory acidosis and K depletion is consistent with the hypothesis that intracellular acidification may participate in the stimulation of ammoniagenesis. The finding of a normal renal pHi in chronic respiratory acidosis, which does not stimulate ammoniagenesis in the rat, further supports this hypothesis.