Mercury blockade of thiazide-sensitive NaCl cotransport in flounder urinary bladder.
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.
Wilkinson
D J
DJ
Mount Desert Island Biological Laboratory, Salsbury Cove, Maine.
Post
M A
MA
Venglarik
C
C
Chang
D
D
Dawson
D C
DC
D000818:Animals; D001581:Benzothiadiazines; D004232:Diuretics; D005432:Flounder; D066298:In Vitro Techniques; D017136:Ion Transport / Q000187:drug effects; D008628:Mercury / Q000633:toxicity*; D011188:Potassium / Q000378:metabolism; D012965:Sodium Chloride / Q000378:metabolism*; D049993:Sodium Chloride Symporter Inhibitors / Q000494:pharmacology*; D001743:Urinary Bladder / Q000187:drug effects / Q000378:metabolism*
D001581:Benzothiadiazines; D004232:Diuretics; D049993:Sodium Chloride Symporter Inhibitors; D012965:Sodium Chloride; D008628:Mercury; D011188:Potassium