The induction of an ATP-sensitive K(+) current in cardiac myocytes of air- and water-breathing vertebrates

Opening of ATP-sensitive potassium channels (K(ATP)) is an effective cardioprotective mechanism in mammals. The amplitude of the ATP-sensitive K(+) current (I(K,ATP)) and the opening sensitivity of K(ATP) channels are, however, poorly known in ectotherms. As O(2)-sensing mechanisms and reactions to O(2) deficiency differ in aquatic and terrestrial animals, we hypothesised that the response of K(ATP) channels to metabolic inhibition would be different between air- and water-breathers. We therefore compared I(K,ATP) in ventricular myocytes of an anoxia-sensitive (Oncorhynchus mykiss) and an anoxia-tolerant fish (Carassius carassius), two amphibians (Xenopus laevis and Rana temporaria) and a terrestrial reptile (Lacerta vivipara) using the whole-cell patch-clamp method. I(K,ATP) was induced by preventing mitochondrial and/or glycolytic ATP production and perfusing myocytes with an ATP-free pipette solution. All species had a glibenclamide-sensitive I(K,ATP), but the current amplitude was much greater in air-breathers than in water-breathers. Furthermore, the I(K,ATP) in air-breathers was more sensitive to intracellular ATP depletion than in water-breathing animals. These findings indicate that I(K,ATP) is larger and more easily induced in air- than water-breathers. In all ectotherms, the first response to complete metabolic inhibition was the induction of a large inward current, the amplitude of which exceeded that of I(K,ATP). Thus, the protective effect of the I(K,ATP) may be physiologically significant only during partial metabolic blockade.