Chloride conductance in human atrial cells

Sakai, Rieko; Hagiwara, Nobuhisa; Kasanuki, Hiroshi; Hosoda, Saichi

doi:10.1016/s0022-2828(95)92199-0

Cited by 41 publications

(27 citation statements)

References 12 publications

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“…Molecular analysis strongly suggests that these cells express an alternatively spliced variant of the CFTR channel (Horowitz et al, 1993;Hart et al, 1996). Although an initial report suggested that CFTR is expressed in human cardiac tissue (Levesque et al, 1992), other studies have failed to identify a cAMP-dependent Cl Ϫ current in human cardiac myocytes (Oz and Sorota, 1995;Sakai et al, 1995). If present in the human heart, the CFTR channel could play an important role in controlling the action potential duration.…”

Section: Discussionmentioning

confidence: 99%

Arylaminobenzoate Block of the Cardiac Cyclic AMP-Dependent Chloride Current

Walsh

Wang

1998

Mol Pharmacol

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The cystic fibrosis transmembrane conductance regulator (CFTR) Cl Ϫ channel has been identified in the cardiac muscle of a number of mammalian species, including humans. The goal of this study was to begin quantifying the structural requirements necessary for arylaminobenzoate block of the CFTR channel. The cardiac cAMP-dependent Cl Ϫ current (I Cl ) was measured using the whole-cell arrangement of the patch-clamp technique in guinea pig ventricular myocytes during stimulation of protein kinase A with forskolin. At drug concentrations below the IC 50 value for channel block, reduction of I Cl by the arylaminobenzoates occurred in a strongly voltage-dependent manner with preferential inhibition of the inward currents. At higher drug concentrations, block of both the inward and outward I Cl was observed. Increasing the length of the carbon chain between

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Section: Discussionmentioning

confidence: 99%

Arylaminobenzoate Block of the Cardiac Cyclic AMP-Dependent Chloride Current

Walsh

Wang

1998

Mol Pharmacol

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“…I Cl,swell is found in normal cells from a number of species 31 including humans. 6,7,32,33 Sorota 18 found that 9AC blocked by 50%, whereas niflumic acid completely blocked I Cl,swell at all voltages. Block by 4,4Ј-dinitrostilbene-2,2Ј-disulfonic acid (DNDS) was voltage dependent, with only partial block at negative voltages and complete block at membrane voltages Ͼ0 mV.…”

Section: Characteristics Of I Clswellmentioning

confidence: 97%

“…6,7 This current has been termed I Cl,swell . Several molecules have been postulated to function as swelling-activated Cl -channels or channel regulators including ClC-2, 8 PICln, 9,10 P-glycoprotein, 11,12 and phospholemman.…”

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confidence: 99%

Swelling-Activated Chloride Current Is Persistently Activated in Ventricular Myocytes From Dogs With Tachycardia-Induced Congestive Heart Failure

Clemo

Stambler

Baumgarten

1999

Circulation Research

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Abstract-The hypothesis that cellular hypertrophy in congestive heart failure (CHF) modulates mechanosensitive (ie, swelling-or stretch-activated) anion channels was tested. Digital video microscopy and amphotericin-perforated-patch voltage clamp were used to measure cell volume and ion currents in ventricular myocytes isolated from normal dogs and dogs with rapid ventricular pacing-induced CHF. In normal myocytes, osmotic swelling in 0.9T to 0.6T solution (T, relative osmolarity; isosmotic solution, 296 mOsmol/L) was required to elicit I Cl,swell , an outwardly rectifying swelling-activated Cl -current that reversed near -33 mV and was inhibited by 1 mmol/L 9-anthracene carboxylic acid (9AC), an anion channel blocker. Block of I Cl,swell by 9AC simultaneously increased the volume of normal cells in hyposmotic solutions by up to 7%, but 9AC had no effect on volume in isosmotic or hyperosmotic solutions. In contrast, I Cl,swell was persistently activated under isosmotic conditions in CHF myocytes, and 9AC increased cell volume by 9%. Osmotic shrinkage in 1.1T to 1.5T solution inhibited both I Cl,swell and 9AC-induced cell swelling in CHF cells, whereas osmotic swelling only slightly increased I Cl,swell . The current density for fully activated 9AC-sensitive I Cl,swell was 40% greater in CHF than normal myocytes. In both groups, 9AC-sensitive current and 9AC-induced cell swelling were proportional with changes in osmolarity and 9AC concentration, and the effects of 9AC on current and volume were blocked by replacing bath Cl -with methanesulfonate. CHF thus altered the set point and magnitude of I Cl,swell and resulted in its persistent activation. We previously observed analogous regulation of mechanosensitive cation channels in the same CHF model. Mechanosensitive anion and cation channels may contribute to the electrophysiological and contractile derangements in CHF and may be novel targets for therapy. (Circ Res. 1999;84:157-165.)

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“…Messenger RNA for CFTR has been detected in whole tissue from human atrium and ventricle [14,29]. Most whole-cell patchclamp studies have not detected CFTR current in human atrium [2,15,18,19,30] (but see [29]). There is only one published report that looked for CFTR current in human ventricle.…”

Section: Introductionmentioning

confidence: 99%

Paucity of CFTR current but modest CFTR immunoreactivity in non-diseased human ventricle

Finley

Sorota

2000

Pflugers Arch - Eur J Physiol

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We looked for evidence of expression of the cystic fibrosis transmembrane conductance regulator (CFTR) in non-diseased human ventricle. In rabbit and guinea pig the CFTR current is present in the highest density in subepicardial ventricular myocytes. In the present study, whole-cell patch-clamp was used to determine if a CFTR-like chloride current (I(CFTR,card)) can also be activated in human subepicardial ventricular myocytes. No evidence for I(CFTR,card) was detected in these electrophysiological studies when 10 microM forskolin was applied to 23 different cells from 4 donor hearts. Consistent with our previous results, a swelling-induced chloride current (I(Cl,swell)) could be observed after cell inflation. The enzymatic digestion of human ventricle to release single myocytes may have affected our ability to detect I(CFTR,card). Therefore, we looked for anti-CFTR immunoreactivity in slices of left ventricular free wall. A strong immunoreactivity signal was observed in guinea pig ventricle, a positive control. Background staining levels were seen in dog ventricle, a negative control tissue. Human anti-CFTR immunoreactivity was slightly above background. This low level of anti-CFTR immunoreactivity is consistent both with reports that CFTR mRNA is detectable in human ventricle and our inability to detect a significant I(CFTR,card) current density.

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Chloride conductance in human atrial cells

Cited by 41 publications

References 12 publications

Arylaminobenzoate Block of the Cardiac Cyclic AMP-Dependent Chloride Current

Arylaminobenzoate Block of the Cardiac Cyclic AMP-Dependent Chloride Current

Swelling-Activated Chloride Current Is Persistently Activated in Ventricular Myocytes From Dogs With Tachycardia-Induced Congestive Heart Failure

Paucity of CFTR current but modest CFTR immunoreactivity in non-diseased human ventricle

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