Effects of inorganic mercury (HgCl2) on electrical excitability of rainbow trout (Oncorhynchus mykiss) heart.

Abstract

Mercury (Hg) is a major environmental pollutant that is toxic to fish. One of its targets is the heart, but its mode of action on the electrical excitability of fish heart is poorly known. To address this, we investigated the acute effects of inorganic mercury (Hg2+) on the heart of rainbow trout (Oncorhynchus mykiss) at three levels of biological organization: (a) electrocardiogram of perfused whole hearts ex vivo (the whole heart level), (b) action potentials (APs; the cellular level), and (c) ion channel currents of isolated ventricular myocytes (molecular level). Whole hearts and myocytes were exposed to 0.1-10 µM HgCl2. In ventricular myocytes, Hg2+ inhibited L-type Ca2+ (ICaL) and fast Na+ current (INa), the two major inward (depolarizing) currents of fish hearts, in a concentration-dependent manner. The INa and ICaL were inhibited with half-maximal effect (IC50 value) at 0.2 ± 0.04 and 0.7 ± 0.08 µM, respectively. Of the two major outward (repolarizing) K+ currents, IKr was inhibited in a concentration-dependent manner with an IC50 value of 1.0 ± 0.1 µM, while IK1 current was totally resistant to Hg2+. The inhibition of sarcolemmal ion currents caused prominent changes in the shape of ventricular AP. Action potential duration at 50% and 90% (APD50, APD90) level of repolarization was prolonged, while the early plateau (APD10) was markedly shortened. The long plateau phase was accompanied by early and delayed afterdepolarizations, leading to triggered APs. At the level of perfused whole hearts, the molecular and cellular level changes appeared as arrhythmias that were characterized by bradycardia, atrioventricular block, prolongation the duration of ventricular AP and triggered activity. Cardiotoxicity of Hg2+ can weaken cardiac function in fish. This effect may be exacerbated when combined with high temperature stress, as both factors have a similar mode of action.