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 (KATP) 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 KATP antagonist, to aldosterone superfusion abolished these effects different to sodium 5-hydroxydecanoate, a mitochondrial-KATP 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-KATP channels may be involved in this context.
*Department of Cardiology, CHU de Caen, Caen, France;
†Research Unit Signalisation, Électrophysiologie et Imagerie des Lésions d'Ischémie-Reperfusion Myocardique, Université de Caen Basse-Normandie, Caen, France;
‡Department of Cardiovascular Sciences, Sapienza University, Rome, Italy; and
§Université de Caen Basse-Normandie, Medical School, Caen, France.
Reprints: Joachim Alexandre, MD, Department of Cardiology, CHU de Caen, Avenue de la côte de nacre, Caen F-14000, France (e-mail: email@example.com).
The authors report no conflicts of interest.
J. Alexandre was supported by the Fédération Française de Cardiologie.
Received February 15, 2014
Accepted March 11, 2014