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Evidence against a contribution by Na(+)‐Cl‐ cotransport to chloride accumulation in rat arterial smooth muscle.
Author(s) -
Davis J P
Publication year - 1996
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.1996.sp021196
Subject(s) - bumetanide , hyperpolarization (physics) , chemistry , cotransporter , chlorothiazide , chloride , biophysics , endocrinology , medicine , sodium , diuretic , membrane potential , acetazolamide , biochemistry , stereochemistry , biology , organic chemistry , nuclear magnetic resonance spectroscopy
1. Chloride accumulation into rat saphenous arterial smooth muscle has been examined using chloride‐sensitive microelectrodes, to assess the contribution of Na(+)‐Cl‐cotransport. 2. Bumetanide (10 microM) produced a fall in intracellular chloride ([Cl‐]i), and a hyperpolarization of membrane potential (Em). However, [Cl‐]i remained above the equilibrium level predicted from the membrane potential, indicating a residual accumulation. 3. Replacement of extracellular sodium with N‐methyl‐D‐glucamine or choline caused a fall in [Cl‐]i similar to that observed with bumetanide, but the hyperpolarization of Em was larger. In Na(+)‐free media, bumetanide had no effect. [Cl‐]i remained significantly above equilibrium. 4. In the presence of bumetanide, chlorothiazide produced a further dose‐dependent fall in [Cl‐]i, and hyperpolarization of Em. However, although [Cl‐]i fell more than with bumetanide alone, it remained significantly above equilibrium. Metolazone was without effect at 100 microM. 5. In the presence of bumetanide, ethacrynic acid and N‐ethyl maleimide caused a dose‐dependent hyperpolarization of Em and a fall in [Cl‐]i to equilibrium. 6. The third inward chloride pump in rat saphenous arterial smooth muscle appears not to be a form of Na(+)‐Cl‐ cotransport. The potency series of thiazide diuretic action (acetazolamide > chlorothiazide > metolazone) differed significantly from that published for Na(+)‐Cl‐ cotransport, and there is no sodium dependence.