An autocrine role for endothelin-1 in the regulation of proximal tubule NHE3

Christoph Licht, Kamel Laghmani, Masashi Yanagisawa, Patricia A. Preisig, Robert J. Alpern

Research output: Contribution to journalArticlepeer-review

33 Scopus citations

Abstract

Background. Chronic metabolic acidosis leads to an increase in NHE3 activity that is mediated by endothelin-1 (ET-1) expression and activation of the proximal tubule endothelin B receptor. Chronic metabolic acidosis increases preproET-1 mRNA abundance in kidney cortex, but the cell responsible has not been identified. Methods. PreproET-1 mRNA abundance was quantified by competitive reverse transcription-polymerase chain reaction (RT-PCR) on tissue harvested from control rats or rats in which chronic metabolic acidosis was induced by addition of NH4Cl to the drinking water. Results. Chronic metabolic acidosis leads to an increase in preproET-1 mRNA expression in kidney cortex, proximal tubules, and glomeruli. The increase in preproET-1 expression correlates with the decrease in blood [HCO3-]. ET-1 expression is also increased by acidosis in abdominal aorta, but not in cardiac muscle. Conclusion. In the renal proximal tubule, chronic metabolic acidosis induces an increase in preproET-1 expression, providing a mechanism for autocrine regulation of proximal tubule NHE3 activity. This response is not unique to the proximal tubule cell, but is also not ubiquitous.

Original languageEnglish (US)
Pages (from-to)1320-1326
Number of pages7
JournalKidney international
Volume65
Issue number4
DOIs
StatePublished - Apr 2004

Keywords

  • Aorta
  • Autocrine regulation
  • Chronic metabolic acidosis
  • Heart
  • Na/H antiporter

ASJC Scopus subject areas

  • Nephrology

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