Sodium-independent inward cl pumping in rat cardiac ventricular
cells.
Chipperfield, Alan R., Julian P. L. Davis, and Alexander A. Harper.
Department of Anatomy and Physiology, The University of Dundee,
Dundee DD1 4HN
APStracts 3:0391H, 1996.
Intracellular [Cl] in rat cardiac ventricular muscle, measured with
double-barrelled microelectrodes in vitro, was 21.3 ( 1.5 (s.d, n =
47) mM. With the (Na+K+Cl) cotransport inhibitor, 10 (M bumetanide,
it fell to 13.4 ( 1.4 (n = 27) mM and with 1 mM acetazolamide also it
fell further to 7.2 ( 1.5 (n = 5) mM, close to equilibrium with Em.
In the absence of Na, [Cl]i was 15.9 ( 1.4 (n = 8) and with 1 mM
acetazolamide it fell to 6.5 ( 0.6 (n = 4), again close to
equilibrium. The bumetanide- and Na-insensitive component of inward
Cl pumping was inhibited by chlorothiazide and ethacrynic acid but
unaffected by the (Na+Cl) cotransport inhibitor, metolazone. There
was inhibition of (Na+K+Cl) cotransport by chlorothiazide =
acetazolamide > metolazone. The anion exchange inhibitor, DIDS,
and HCO3 had no effect on [Cl]i in any condition. Thus, Cl
accumulation in rat ventricle is fully accounted for by two systems,
namely, (Na+K+Cl) cotransport and a Na-independent, possibly primary
active, process.
Received 11 March 1996; accepted in final form 21 August 1996.
APS Manuscript Number H232-6.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 19 September 1996