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Titolo:
Modulation of cardiac Na+ current by gadolinium, a blocker of stretch-induced arrhythmias
Autore:
Li, GR; Baumgarten, CM;
Indirizzi:
Virginia Commonwealth Univ, Med Coll Virginia, Dept Physiol, Richmond, VA 23298 USA Virginia Commonwealth Univ Richmond VA USA 23298 , Richmond, VA 23298 USA
Titolo Testata:
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
fascicolo: 1, volume: 280, anno: 2001,
pagine: H272 - H279
SICI:
0363-6135(200101)280:1<H272:MOCNCB>2.0.ZU;2-G
Fonte:
ISI
Lingua:
ENG
Soggetto:
ISOLATED VENTRICULAR MYOCYTES; ACTIVATED ION CHANNELS; CALCIUM CHANNELS; PURKINJE-CELLS; GUINEA-PIG; EXTRACELLULAR DIVALENT; VOLUME REGULATION; XENOPUS OOCYTES; SURFACE-CHARGE; CATION CURRENT;
Keywords:
lanthanides; mechanoelectrical feedback; mechanosensitive channels;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
41
Recensione:
Indirizzi per estratti:
Indirizzo: Baumgarten, CM Virginia Commonwealth Univ, Med Coll Virginia, Dept Physiol, 1101 E Marshall St, Richmond, VA 23298 USA Virginia Commonwealth Univ 1101 E Marshall St Richmond VA USA 23298
Citazione:
G.R. Li e C.M. Baumgarten, "Modulation of cardiac Na+ current by gadolinium, a blocker of stretch-induced arrhythmias", AM J P-HEAR, 280(1), 2001, pp. H272-H279

Abstract

Gd3+ blocks stretch-activated channels and suppresses stretch-induced arrhythmias. We used whole cell voltage clamp to examine whether effects on Nachannels might contribute to the antiarrhythmic efficacy of Gd3+. Gd3+ inhibited Na+ current (I-Na) in rabbit ventricle (IC50 = 48 muM at -35 mV, holding potential -120 mV), and block increased at more negative test potentials. Gd3+ made the threshold for INa more positive and reduced the maximum conductance. Gd3+ (50 muM) shifted the midpoints for activation and inactivation of I-Na 7.9 and 5.7 mV positive but did not alter the slope factor foreither relationship. Activation and inactivation kinetics were slowed in amanner that could not be explained solely by altered surface potential. Paradoxically, Gd3+ increased I-Na under certain conditions. With membrane potential held at -75 mV, Gd3+ still shifted threshold for activation positive, but INa increased positive to -40 mV, causing the current-voltage curvesto cross over. When availability initially was low, increased availabilityinduced by Gd3+ dominated the response at test potentials positive to -40 mV. The results indicate that Gd3+ has complex effects on cardiac Na+ channels. Independent of holding potential, Gd3+ is a potent I-Na blocker near threshold potential, and inhibition of I-Na by Gd3+ is likely to contribute to suppression of stretch-induced arrhythmias.

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Documento generato il 23/09/20 alle ore 13:58:25