Mercury blockade of thiazide-sensitive NaCl cotransport in flounder urinary bladder

Daniel J. Wilkinson, Marc A. Post, Charles Venglarik, Dean Chang, David C. Dawson

Research output: Contribution to journalArticle

5 Scopus citations

Abstract

The effects of HgCl2 on ion transport were investigated using isolated sheets of flounder urinary bladder, a model epithelium that is capable of electrically silent NaCl absorption and electrogenic K secretion. Exposure of the mucosal surface of the bladder to submicromolar doses of HgCl2 reduced K secretion, but the effect was not due to blockade of apical K channels. Rather, the effects of HgCl2 were virtually identical to those seen with experimental maneuvers that blocked the thiazide-sensitive NaCl cotransporter in the apical membrane, e.g., hydrochlorothiazide, Cl-free solutions, and Na-free solutions. Mucosal HgCl2 also blocked 22Na absorption, suggesting that the effect of the metal was mediated by blockade of NaCl entry. The effects of HgCl2 had a rapid onset and were readily reversed by washing, suggesting a noncovalent binding reaction. The abundance of polyanionic Hg complexes in salt solutions prompts the speculation that one of these may bind to the Cl-binding site on the cotransporter, thereby blocking it. The results provide the first evidence that the thiazide-sensitive NaCl cotransporter is a specific site of action for inorganic mercury.

Original languageEnglish (US)
Pages (from-to)170-176
Number of pages7
JournalToxicology and Applied Pharmacology
Volume123
Issue number1
DOIs
StatePublished - Nov 1993

ASJC Scopus subject areas

  • Toxicology
  • Pharmacology

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