ArticlePflugers Archiv : European journal of physiology1993
Effect of parathyroid hormone on acid/base transport in rabbit renal proximal tubule S3 segment.
Article in Pflugers Archiv : European journal of physiology, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 15 citations in OpenAlex.
- Chloride transport in the renal proximal tubule.Pflugers Archiv : European journal of physiology · 2004Review
- Activation of the basolateral Cl- conductance by cAMP in rabbit renal proximal tubule S3 segments.Pflugers Archiv : European journal of physiology · 1995Article
- Evidence for conductive Cl- pathway in the basolateral membrane of rabbit renal proximal tubule S3 segment.The Journal of clinical investigation · 1993Article
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Authors and funding
5 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
The effect of parathyroid hormone (PTH) on acid/base transport in isolated rabbit renal proximal tubule S3 segment was investigated with double-barreled and conventional microelectrodes. PTH (10 nM) induced a small depolarization and enhanced the initial rates of cell pH (pHi) increase and cell Cl- ([Cl-]i) decrease in response to bath Cl- removal by 28.0 +/- 2.1% and 31.0 +/- 6.4% respectively. The calculated initial HCO3- influx to bath Cl- removal was also enhanced by 28%. On the other hand, PTH reduced the initial rate of pHi decrease to luminal Na+ removal in the absence of HCO3-/CO2 by 20.4 +/- 3.9%. The PTH-induced depolarization was not accompanied with changes in steady-state pHi or [Cl-]i levels, but was greatly attenuated in the presence of ouabain (0.1 mM). Either dibutyryl-cAMP (0.1 mM) plus theophylline (1 mM) or forskolin (10 microM) alone could reproduce all the effects of PTH. These results indicate that (a) PTH inhibits the luminal Na+/H+ exchanger but stimulates the basolateral Cl-/HCO3- exchanger in the S3 segment; (b) the PTH-induced depolarization largely results from inhibition of Na+/K(+)-ATPase and (c) all these effects are at least partly mediated by a cAMP-dependent mechanism.
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