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Titolo:
Swelling-activated chloride current is persistently activated in ventricular myocytes from dogs with tachycardia-induced congestive heart failure
Autore:
Clemo, HF; Stambler, BS; Baumgarten, CM;
Indirizzi:
Virginia3298monwealth Univ, Med Coll Virginia, Dept Physiol, Richmond, VA 2 Virginia Commonwealth Univ Richmond VA USA 23298 Physiol, Richmond, VA 2 Virginia Commonwealth Univ, Med Coll Virginia, Dept Internal Med, Richmond, Virginia Commonwealth Univ Richmond VA USA 23298 Internal Med, Richmond, Case Western Reserve Univ, Div Cardiol, Cleveland, OH 44106 USA Case Western Reserve Univ Cleveland OH USA 44106 Cleveland, OH 44106 USA Univ Hosp Cleveland, Cleveland, OH 44106 USA Univ Hosp Cleveland Cleveland OH USA 44106 eland, Cleveland, OH 44106 USA
Titolo Testata:
CIRCULATION RESEARCH
fascicolo: 2, volume: 84, anno: 1999,
pagine: 157 - 165
SICI:
0009-7330(19990205)84:2<157:SCCIPA>2.0.ZU;2-F
Fonte:
ISI
Lingua:
ENG
Soggetto:
PROTEIN-KINASE-C; OVERLOAD CARDIAC-HYPERTROPHY; RESISTANCE P-GLYCOPROTEIN; ATRIAL-NATRIURETIC-FACTOR; CELL-VOLUME; SIGNAL-TRANSDUCTION; CHANNEL; EXPRESSION; CONDUCTANCE; RAT;
Keywords:
arrhythmia; cardiomyopathy; cardiac edema; cell size; ion channel gating;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
54
Recensione:
Indirizzi per estratti:
Indirizzo: Clemo, HF Virginiachmond,wealth Univ, Med Coll Virginia, Dept Physiol, POB980551, Ri Virginia Commonwealth Univ POB 980551 Richmond VA USA 23298 , Ri
Citazione:
H.F. Clemo et al., "Swelling-activated chloride current is persistently activated in ventricular myocytes from dogs with tachycardia-induced congestive heart failure", CIRCUL RES, 84(2), 1999, pp. 157-165

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-patchvoltage 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 requiredto elicit I-Cl,I-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,I-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,I-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,I-swell and 9AC-induced cell swelling in CHF cells, whereas osmotic swelling only slightlyincreased I-Cl,I-swell. The current density for fully activated 9AC-sensitive I-Cl,I-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,I-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.

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Documento generato il 19/09/20 alle ore 08:30:36