Proarrhythmic Effects of Aldosterone During Myocardial Ischemia-Reperfusion: Implication of the Sarcolemmal-KATP Channels

Objective: To assess the electrophysiological impact of aldosterone during myocardial ischemia-reperfusion. Methods: We used an in vitro model of "border zone" using rabbit right ventricle and standard microelectrodes. Results: Aldosterone (10 and 100 nmol/L) shortened ischemic action potential [action potential duration at 90% of repolarization (APD(90)), 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 APD(90) shortening. Aldosterone (10 and 100 nmol/L) increased APD(90) 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. Conclusions: In this in vitro rabbit model of border zone, aldosterone induced RMP hyperpolarization and decreased ischemic APD(90) 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.