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Titolo:
Effects of endothelin-1 on K+ currents from rat ventricular myocytes
Autore:
James, AF; Ramsey, JE; Reynolds, AM; Hendry, BM; Shattock, MJ;
Indirizzi:
Univ Bristol, Sch Med Sci, Dept Physiol, Bristol BS8 1TD, Avon, England Univ Bristol Bristol Avon England BS8 1TD Bristol BS8 1TD, Avon, England Univ Bristol, Sch Med Sci, Cardiovasc Res Labs, Bristol BS8 1TD, Avon, England Univ Bristol Bristol Avon England BS8 1TD Bristol BS8 1TD, Avon, England Univ London Kings Coll, GKT Sch Med, Dept Renal Med, Cell Signaling Grp, London SE5 9PJ, England Univ London Kings Coll London England SE5 9PJ p, London SE5 9PJ, England St Thomas Hosp, Rayne Inst, Ctr Cardiovasc Biol & Med, London SE1 7EH, England St Thomas Hosp London England SE1 7EH iol & Med, London SE1 7EH, England
Titolo Testata:
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
fascicolo: 4, volume: 284, anno: 2001,
pagine: 1048 - 1055
SICI:
0006-291X(20010622)284:4<1048:EOEOKC>2.0.ZU;2-5
Fonte:
ISI
Lingua:
ENG
Soggetto:
PROTEIN-KINASE-C; ACTION-POTENTIAL DURATION; CARDIAC MYOCYTES; POTASSIUM CURRENT; MOLECULAR DIVERSITY; RECEPTOR ANTAGONIST; ARACHIDONIC-ACID; CA2+ TRANSIENT; HUMAN HEART; I-TO;
Keywords:
endothelin-1; PD 142893; G-protein-coupled receptors; potassium current; transient outward current; steady-state K+ current; background K+ current; cardiac myocytes; patch clamp;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
46
Recensione:
Indirizzi per estratti:
Indirizzo: James, AF Univ Bristol, Sch Med Sci, Dept Physiol, Univ Walk, Bristol BS8 1TD, Avon,England Univ Bristol Univ Walk Bristol Avon England BS8 1TD Avon,England
Citazione:
A.F. James et al., "Effects of endothelin-1 on K+ currents from rat ventricular myocytes", BIOC BIOP R, 284(4), 2001, pp. 1048-1055

Abstract

It has been suggested that the positive inotropic effect of the vasoactivepeptide hormone, endothelin-1 (ET-1), involves inhibition of cardiac K+ currents. In order to identify the K+ currents modulated by ET-I, the outwardK+ currents of isolated rat ventricular myocytes were investigated using whole-cell patch-clamp recording techniques. Outward currents were elicited by depolarisation to +40 mV for 200 ms from the holding potential of -60 mV, Currents activated rapidly, reaching a peak (I-pk) Of 1310 +/- 115 PA andsubsequently inactivating to an outward current level of 1063 +/- 122 PA at the end of the voltage-pulse (I-late) (n = II). ET-I (20 nM) reduced I-pkby 247.6 +/- 60 7 PA (n = II, P < 0.01) and reduced I-late by 323.2 +/- 43.9 pA (P < 0.001). The effects of ET-1 were abolished in the presence of the nonselective ET receptor antagonist, PD 142893 (10 muM, n = 5). Outward currents were considerably reduced and the effects of ET-I were not observedwhen K+ was replaced with Cs+ in the experimental solutions; this indicates that ET-I modulated K+-selective currents. a double-pulse protocol was used to investigate the inactivation of the currents. The voltage-dependent inactivation of the currents from potentials positive to -80 mV was fitted by a Boltzmann equation revealing the existence of an inactivating transientoutward component (I-to) and a noninactivating steady-state component (I-ss), ET-1 markedly inhibited I-ss by 43.0 +/- 3.8% (P < 0.001, n = 7) and shifted the voltage-dependent inactivation of I-to by +3.3 +/- 1.2 mV (P < 0.05). Although ET-I had little effect on the onset of inactivation of the currents elicited from a conditioning potential of -70 mV, the time-independent noninactivating component of the currents was markedly inhibited. In conclusion, the predominant effect of ET-1 was to inhibit a noninactivating steady-state background K+ current (I-ss). These results are consistent with the hypothesis that I-ss inhibition contributes to the inotropic effects ofET-I, (C) 2001 Academic Press.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 01/04/20 alle ore 11:49:49