Sodium-independent inward chloride pumping in rat cardiac ventricular cells

• Published in: The American journal of physiology Vol. 272; no. 2 Pt 2; pp. H735 - H739
• Main Authors: Chipperfield, A R, Davis, J P, Harper, A A
• Format: Journal Article
• Language: English
• Published: United States 01-02-1997
• Subjects: Acetazolamide - pharmacology; Animals; Anions - metabolism; Carrier Proteins - antagonists & inhibitors; Chlorides - metabolism; Ethacrynic Acid - pharmacology; Heart Ventricles; Intracellular Membranes - drug effects; Intracellular Membranes - metabolism; Ion Exchange; Male; Membrane Potentials; Myocardium - cytology; Myocardium - metabolism; Osmolar Concentration; Rats; Rats, Sprague-Dawley; Sodium - pharmacology; Sodium - physiology; Sodium Chloride Symporters; Symporters; Ventricular Function - drug effects
• ISSN: 0002-9513
• DOI: 10.1152/ajpheart.1997.272.2.H735

The intracellular Cl concentration ([Cl]i) in rat cardiac ventricular muscle, measured with double-barreled microelectrodes in vitro, was 21.3 +/- 1.5 (SD) mM [number of observations (n) = 46]. With the Na-K-Cl cotransport inhibitor bumetanide (10 microM), it fell to 13.4 +/- 1.4 mM (n = 27), and with 1 mM acetazolamide, it fell further, to 7.2 +/- 1.5 mM (n = 5), close to equilibrium with the membrane potential. In the absence of Na, [Cl]i was 15.9 +/- 1.4 mM (n = 8), and with 1 mM acetazolamide, it fell to 6.5 +/- 0.6 mM (n = 4), again close to equilibrium. The bumetanide- and Na-insensitive components of inward Cl pumping were inhibited by chlorothiazide and ethacrynic acid but were unaffected by the Na-Cl cotransport inhibitor metolazone. There was inhibition of Na-K-Cl cotransport by chlorothiazide = acetazolamide > metolazone. The anion exchange inhibitor 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid and HCO3 had no effect on [Cl]i in any condition. Thus Cl accumulation in the rat ventricle is fully accounted for by two systems, namely, Na-K-Cl cotransport and an Na-independent, possibly primary active, process.