Luminal secretion of ammonia in the mouse proximal tubule perfused in vitro.

@article{Nagami1988LuminalSO,
  title={Luminal secretion of ammonia in the mouse proximal tubule perfused in vitro.},
  author={Glenn T. Nagami},
  journal={The Journal of clinical investigation},
  year={1988},
  volume={81 1},
  pages={
          159-64
        }
}
  • G. Nagami
  • Published 1988
  • Biology
  • The Journal of clinical investigation
A major portion of the total ammonia (tNH3 = NH3 + NH+4) produced by the isolated perfused mouse proximal tubule is secreted into the luminal fluid. To assess the role of Na+-H+ exchange in net tNH3 secretion, rates of net tNH3 secretion and tNH3 production were measured in proximal tubule segments perfused with control pH 7.4 Krebs-Ringer bicarbonate (KRB) buffer or with modified KRB buffers containing 10 mM sodium and 0.1 mM amiloride. Net tNH3 secretion was inhibited by 90% in proximal… 
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It is demonstrated that isolated, perfused mouse S3 proximal tubule segments produce and secrete ammonia, that NH4Cl-induced acidosis does not affect the basal rates of ammonia production and secretion, and that ANG II, added to the luminal fluid, stimulates ammoniaProduction and secretion to a greater extent in S3 segments from acidotic mice.
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  • 1990
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It is suggested that luminal potassium concentration has a direct effect on cell-to-lumen transport of ammonia in a way that was independent of total ammonia production rates, independent of Na(+)-H+ exchange activity, and not due to changes in transepithelial fluxes oftotal ammonia.
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It is demonstrated that a 7-day acid challenge induces an adaptive increase in ammonia production and secretion by the proximal tubule and suggested that during metabolic acidosis, angiotensin II signaling is necessary for adaptive enhancements of ammonia excretion by the kidney and ammonia productionand secretion by S2 proximal Tubule segments, as mediated, in part, by ang Elliotensin receptor-dependent enhancement of NHE3 expression.
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