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Titolo:
PLASMALOGEN-DERIVED LYSOLIPID INDUCES A DEPOLARIZING CATION CURRENT IN RABBIT VENTRICULAR MYOCYTES
Autore:
CALDWELL RA; BAUMGARTEN CM;
Indirizzi:
VIRGINIA COMMONWEALTH UNIV,MED COLL VIRGINIA,DEPT PHYSIOL,BOX 980551 RICHMOND VA 23298 VIRGINIA COMMONWEALTH UNIV,MED COLL VIRGINIA,DEPT PHYSIOL RICHMOND VA23298
Titolo Testata:
Circulation research
fascicolo: 5, volume: 83, anno: 1998,
pagine: 533 - 540
SICI:
0009-7330(1998)83:5<533:PLIADC>2.0.ZU;2-6
Fonte:
ISI
Lingua:
ENG
Soggetto:
ISCHEMIC HUMAN MYOCARDIUM; ACTIVATED ION CHANNELS; LYSOPHOSPHATIDYLCHOLINE ACCUMULATION; MEMBRANE FLUIDITY; SODIUM CURRENT; EXOGENOUS LYSOPHOSPHATIDYLCHOLINE; AMPHIPHILIC COMPOUNDS; CARDIAC MYOCYTES; TIME-COURSE; DOG HEART;
Keywords:
PLASMALOGEN; LYSOPHOSPHATIDYLCHOLINE; ISCHEMIA; LANTHANIDE; LYSOPLASMENYLCHOLINE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
46
Recensione:
Indirizzi per estratti:
Citazione:
R.A. Caldwell e C.M. Baumgarten, "PLASMALOGEN-DERIVED LYSOLIPID INDUCES A DEPOLARIZING CATION CURRENT IN RABBIT VENTRICULAR MYOCYTES", Circulation research, 83(5), 1998, pp. 533-540

Abstract

Plasmalogen rather than diacyl phospholipids are the preferred substrate for the cardiac phospholipase A(2) (PLA(2) isoform activated during ischemia. The diacyl metabolite, lysophosphatidylcholine, is arrhythmogenic, but the effects of the plasmalogen metabolite, lysoplasmenylcholine (LPLC), are essentially unknown. We found that 2.5 and 5 mu mol/L LPLC induced spontaneous contractions of intact isolated rabbit ventricular myocytes (median times, 27.4 and 16.4 minutes, respectively) significantly faster than lysophosphatidylcholine (>60 and 37.8 minutes, respectively). Whole-cell recordings revealed that LPLC depolarizedthe resting membrane potential from -83.5+/-0.2 to -21.5+/-1.0 mV. Depolarization was due to a guanidinium toxin-insensitive Na+ influx. The LPLC-induced current reversed at -18.5+/-0.9 mV and was shifted 26.7/-4.2 mV negative by a 10-fold reduction of bath Na+ (Na+/K+ permeability ratio, approximate to 0.12+/-0.06). In contrast, block of Ca2+ channels with Cd2+ and reducing bath Cl- failed to affect the current. The actions of LPLC were opposed by lanthanides. Gd3+ and La3+ were equally effective inhibitors of the LPLC-induced current and equally delayed the onset of spontaneous contractions. However, the characteristics of lanthanide block imply that Gd3+-sensitive, poorly selective, stretch-activated channels were not involved. Instead, the data are consistent with the view that lanthanides increase phospholipid ordering and may thereby oppose membrane perturbations caused by LPLC. Plasmalogens constitute a significant fraction of cardiac sarcolemmal choline phospholipids. In light of their subclass-specific catabolism by phospholipase A, and the present results, it is suggested that LPLC accumulation may contribute to ventricular dysrhythmias during ischemia.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 23/09/20 alle ore 15:25:03