The majority of acute electrical responses to mechanical stimulation of normal myocardium can be mathematically reproduced based on cation-nonselective mechano-sensitive channels (MSC). Relevant responses include mechanical pacing and mechanical termination of ventricular tachyarrhythmias (ILCOR guidelines, Circ Res 2005/112:III1-III54). In order to reproduce the clinically-observed reduced efficacy of mechanical cardioversion in ischaemic heart, mathematical models have to involve an increased contribution from K⁺-selective MSC (Kohl, Bollensdorff & Garny, Exp Physiol, in press). The relevant modelling is based on data from van Wagoner (Circ Res 1993/72: 973–83), showing combined mechano- and ATP-sensitivity of the ATP-inactivated K⁺ current (I_K-ATP ) in atrial cardiomyocyte membrane patches. We therefore conducted experiments on Guinea pig isolated ventricular cardiomyocytes, subjected to metabolic inhibition by FCCP (1 mM) and/or axial stretch. Results show that stretch, applied using two carbon fibres (attached to opposite cell ends; sarcomere length increase by 8-9%), reversibly raises FCCP-induced I_K-ATP (whole-cell patch-clamp, 37°C) by up to 25%, without measurable effects on leak current or reversal potential (-72.9 mV ±2.6 mV, n=5). Thus, application of axial stretch to ventricular cardiomyocytes increases I_K-ATP ; this may underlie the reduced efficacy of mechanical cardioversion in ischaemic heart.