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Titolo:
Modulation of the hyperpolarization-activated inward current (I-f) by antiarrhythmic agents in isolated human atrial myocytes
Autore:
Hoppe, UC; Beuckelmann, DJ;
Indirizzi:
Univ Cologne, Dept Med 3, D-50924 Cologne, Germany Univ Cologne Cologne Germany D-50924 ept Med 3, D-50924 Cologne, Germany
Titolo Testata:
NAUNYN-SCHMIEDEBERGS ARCHIVES OF PHARMACOLOGY
fascicolo: 6, volume: 358, anno: 1998,
pagine: 635 - 640
SICI:
0028-1298(199812)358:6<635:MOTHIC>2.0.ZU;2-E
Fonte:
ISI
Lingua:
ENG
Soggetto:
RABBIT SINOATRIAL NODE; TACHYCARDIA-INDUCED CARDIOMYOPATHY; RADIOFREQUENCY CATHETER ABLATION; HUMAN VENTRICULAR MYOCYTES; TERMINAL HEART-FAILURE; CAT RIGHT ATRIUM; PACEMAKER CURRENT; TRANSCATHETER ABLATION; HYPERTENSIVE RATS; TRANSIENT OUTWARD;
Keywords:
pacemaker current; antiarrhythmic agents; adenosine; carbachol; human atrial myocytes;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
44
Recensione:
Indirizzi per estratti:
Indirizzo: Hoppe, UC Johns Hopkins Univ, 844 Ross Bldg, Baltimore, MD 21205 USA JohnsHopkins Univ 844 Ross Bldg Baltimore MD USA 21205 1205 USA
Citazione:
U.C. Hoppe e D.J. Beuckelmann, "Modulation of the hyperpolarization-activated inward current (I-f) by antiarrhythmic agents in isolated human atrial myocytes", N-S ARCH PH, 358(6), 1998, pp. 635-640

Abstract

The hyperpolarization-activated inward current (I-f) has been discussed tocontribute to arrhythmias in human atrial myocardium. I-f was found to be increased by beta-adrenergic stimulation. In the present study, we evaluatethe modulation of I-f by carbachol, adenosine and by class Ic, III and IV antiarrhythmic drugs in isolated human atrial myocytes. The whole-cell patch-clamp technique was used to record If in isolated myocytes from 18 human right atrial appendages. A typical time- and voltage-dependent hyperpolarization-activated inward current could be recorded in allcells investigated (n=56). Mean current density recorded at -130 mV was -2.8+/-1.2 pApF(-1). Both adenosine and carbachol were found to directly inhibit I-f in human atrial myocytes by shifting the activation curves to more negative potentials. Adenosine 10(-5) mol/l shifted the potential of half-maximal activation by -5.9+/-0.4 mV from -99.4+/-0.6 mV to -105.3+/-0.4 mV (n=8; P<0.05), and carbachol 10-5 mol/l by -5.7+/-0.5 mV from -99.2+/-0.5 mVto -104.9+/-0.6 mV (n=6; P<0.05). The concentration-response curve of adenosine calculated by a Hill function yielded a half-maximal effect of adenosine (EC50) at a concentration of 3.6+/-0.5 mu mol/l, a maximal shift of -6.5+/-0.3 mV, and a Hill coefficient (h) of 2.40. We did not observe any effect of flecainide (10(-5) mol/l; n=8), sotalol (10(-5) mol/l; n=6), amiodarone (10(-5) mol/l; n=6) or verapamil (10(-5) mol/l; n=5) on I-f in human atrial myocytes. However, propafenone (10(-5) mol/l) was found to reversibly reduce I-f current size (9/13 cells) by shifting the activation curve by -5.2+/-0.4 mV (P<0.05). In human atria adenosine- and muscarinic receptor stimulation might function as endogenous protective mechanisms inhibiting the initiation of ectopic tachycardia by reducing I-f current size. Propafenone may be more effective in some patients with atrial tachycardias that do notrespond to other class Ic, III and IV antiarrhythmic drugs. However, it has yet to be defined whether these agents suppress atrial tachycardias via an inhibition of I-f in vivo.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 21/09/20 alle ore 06:24:51