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Proarrhythmic Effects of Aldosterone During Myocardial Ischemia–Reperfusion

2014; Lippincott Williams & Wilkins; Volume: 64; Issue: 2 Linguagem: Inglês

10.1097/fjc.0000000000000097

1533-4023

Joachim Alexandre, Paolo Emilio Puddu, Christophe Simard, Thomas Hof, Laurent Sallé, Romain Guinamard, Alain Manrique, René Rouet, Farzin Beygui, Paul Milliez,

Cardiac electrophysiology and arrhythmias

To assess the electrophysiological impact of aldosterone during myocardial ischemia-reperfusion.We used an in vitro model of "border zone" using rabbit right ventricle and standard microelectrodes.Aldosterone (10 and 100 nmol/L) shortened ischemic action potential [action potential duration at 90% of repolarization (APD90), from 55 ± 3 to 39 ± 1 ms and 36 ± 3 ms, respectively, P < 0.05] and induced resting membrane potential (RMP) hyperpolarization in the nonischemic zone (from -83 ± 1 to -93 ± 7 mV and -94 ± 3 mV, respectively, P < 0.05) and in the ischemic zone during reperfusion (from -81 ± 2 to -88 ± 2 mV and -91 ± 2 mV, respectively, P < 0.05). Bimakalim, an ATP-sensitive potassium (K(ATP)) channel opener, also induced RMP hyperpolarization and APD90 shortening. Aldosterone (10 and 100 nmol/L) increased APD90 dispersion between ischemic and nonischemic zones (from 96 ± 3 to 117 ± 5 ms and 131 ± 6 ms, respectively, P < 0.05) and reperfusion-induced severe premature ventricular contraction occurrence (from 18% to 67% and 75%, respectively, P < 0.05). Adding glibenclamide, a nonspecific K(ATP) antagonist, to aldosterone superfusion abolished these effects different to sodium 5-hydroxydecanoate, a mitochondrial-K(ATP) antagonist.In this in vitro rabbit model of border zone, aldosterone induced RMP hyperpolarization and decreased ischemic APD90 evoking the modulation of K currents. Glibenclamide prevented these effects different to 5-hydroxydecanoate, suggesting that sarcolemmal-K(ATP) channels may be involved in this context.