Intracellular chloride activity in rabbit papillary muscle: effect of serum

1986 ◽  
Vol 64 (11) ◽  
pp. 1381-1384 ◽  
Author(s):  
Jean-Pierre Caillé
Keyword(s):  
Membrane Potential ◽  
Cardiac Cells ◽  
Equilibrium Potential ◽  
Papillary Muscles ◽  
Experimental Conditions ◽  
Intracellular Chloride ◽  
Intracellular Chloride Activity ◽  
Chloride Activity ◽  
Diastolic Potential

The intracellular chloride activity (aiCl), measured with Cl-selective microelectrodes on stimulated rabbit papillary muscles (1 Hz) incubated in serum, was 7.2 ± 2.2 mM (48 measurements). Under the same condition, on the quiescent muscle, aiCl was 7.5 ± 2.8 mM (45 measurements). The membrane potential of quiescent papillary muscles and diastolic potential of stimulated papillary muscles were −79.0 ± 0.7 (50 measurements) and −83.5 ± 0.5 mV (50 measurements), respectively. The experimental conditions were chosen to reproduce the in vivo conditions where the Cl equilibrium potential is close to the membrane potential or to the diastolic potential. After correcting for cytoplasmic interference (4 mM) on the aiCl measurements, the Cl equilibrium potential (ECl) was −84 mV. In conclusion, the Cl distribution in cardiac cells bathed in serum is passive as for in vivo cardiac cells.

Intracellular chloride activity in intact rat liver: relationship to membrane potential and bile flow

1987 ◽  
Vol 252 (5) ◽  
pp. G699-G706
Author(s):  
J. G. Fitz ◽  
B. F. Scharschmidt
Keyword(s):  
Membrane Potential ◽  
Bile Flow ◽  
Chloride Transport ◽  
Basolateral Membrane ◽  
Bile Formation ◽  
Intracellular Chloride ◽  
Canalicular Bile ◽  
Intracellular Chloride Activity ◽  
Chloride Activity

Active chloride transport has been described in a variety of epithelia, and intracellular chloride activity (aiCl) in these tissues is generally elevated twofold or more above the level predicted for passive diffusion. To determine whether active chloride transport might contribute to canalicular bile formation, we have used conventional and Cl- -selective microelectrodes to measure aiCl of rat hepatocytes in vivo under a variety of conditions. Under basal conditions, the membrane potential difference averaged -33.2 +/- 3.5 mV (means +/- SD) in 29 animals, and the ratio (R) of observed aiCl (24.8 mM) to that expected for passive distribution at this membrane potential (22.6 mM) was 1.10 +/- 0.08, a value slightly but significantly greater than that predicted for passive distribution. Infusion of alanine (45-mumol bolus, 10.8-mumol/min infusion) in 5 animals hyperpolarized the membrane potential to -43.6 +/- 4.0 mV over 10-15 min and resulted in a significant fall in aiCl to 15.1 +/- 4.8 mM but with no change in R. Infusion of theophylline (577 nmol/min), taurocholate (3-mumol bolus, 810-nmol/min infusion), and ursodeoxycholic acid (4-mumol bolus, 2.13-mumol/min infusion) into 5 animals each increased bile flow by 6.1, 34.1, and 96.8%, respectively, compared with saline-infused controls but did not alter membrane potential or chloride distribution. These observations indicate that aiCl is close to the level predicted for passive distribution under basal conditions, after hyperpolarization of the membrane potential by alanine, and after stimulation of bile flow by a variety of choleretics. By analogy with Cl- -secreting epithelia, it appears unlikely that active chloride transport across the basolateral membrane contributes significantly to canalicular bile formation by the hepatocyte.

Intracellular chloride activity in mammalian ventricular muscle

1981 ◽  
Vol 241 (3) ◽  
pp. C121-C129 ◽  
Author(s):  
C. M. Baumgarten ◽  
H. A. Fozzard
Keyword(s):  
Papillary Muscle ◽  
Ion Exchange Resin ◽  
Equilibrium Potential ◽  
Sartorius Muscle ◽  
High Potassium ◽  
Intracellular Chloride ◽  
A Value ◽  
Free Media ◽  
Intracellular Chloride Activity ◽  
Chloride Activity

The intracellular chloride activity (formula, see text) of quiescent rabbit right papillary muscle was measured with ion-selective microelectrodes (ISE) made with Corning 477315 liquid ion-exchange resin. The (formula, see text) was 9.8 +/- 2.4 (SD) mM, a value significantly greater than the 6.1 +/- 0.6 mM expected from passive distribution. The chloride equilibrium potential (ECl) was -64.4 +/- 6.6 mV, while membrane potential was -75.9 +/- 2.2 mV and significantly negative to ECl. These values are corrected for a nonchloride signal detected by the ISE. An apparent (formula, see text) of 4.8 +/- 0.6 mM was measured after exposure to Cl-free media for 1 h. Since isotopic chloride was totally washed out by this time, the apparent (formula, see text) in Cl-free media was interpreted as interference and subtracted from the (formula, see text) measured in other media. The conclusion that chloride is not passively distributed is supported by the observation that the (formula, see text) increase in high potassium media was smaller than predicted. In contrast to findings in papillary muscle, (formula, see text) of frog sartorius muscle was consistent with passive distribution, if it is assumed that interference was less than 0.5 mM.

Intracellular chloride activity in quiescent cat papillary muscle

1980 ◽  
Vol 238 (4) ◽  
pp. H487-H493 ◽  
Author(s):  
K. W. Spitzer ◽  
J. L. Walker
Keyword(s):  
Papillary Muscle ◽  
Prolonged Exposure ◽  
Equilibrium Potential ◽  
Cat Papillary Muscle ◽  
Intracellular Chloride ◽  
External Potassium ◽  
Ethanesulfonic Acid ◽  
Intracellular Chloride Activity ◽  
Chloride Activity ◽  
Liquid Ion Exchanger

Intracellular chloride activity (alpha iCl) was measured in quiescent cat papillary muscles with chloride liquid ion-exchanger microelectrodes. Muscles were superfused in bicarbonate-buffered solutions containing a control concentration of chloride (146.1 mM) and either 2.7, 4.4, or 5.4 mM potassium. The resulting mean membrane potentials were -96.2, -86.8, and -80.6 mV, respectively. In contrast, alpha iCl and the chloride equilibrium potential were unchanged by these alterations in external potassium and remained stable at 11 mM and -60 mV for up to 10 h following removal of the tissue from the animal. This value of alpha iCl is approximately 2-4 times greater than that predicted assuming chloride is passively distributed. The upper limit of intracellular interference was estimated from low external chloride superfusion and found to be no greater than 2-3 mM. Prolonged exposure to bicarbonate-free solutions buffered with N-2-hydroxyethyl piperazine-N'-2-ethanesulfonic acid (HEPES) did not reduce the apparent value of alpha iCl, suggesting that intracellular interference from intracellular bicarbonate does not significantly influence the measurement of alpha iCl. These results suggest that chloride can move into cat papillary muscle against an electrochemical gradient.

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