Cell shortening and calcium dynamics in epicardial and encocardial myocytes from the left ventricle of the Goto-Kalizaki type 2 diabetic rats

Abstract

Diabetic cardiomyopathy is considered as one of the major diabetes-associated complications and the pathogenesis of cardiac dysfunction is not well understood. The electromechanical properties of cardiac myocytes vary across the walls of the chambers The aim of this study was to investigate shortening and Ca2+ transport in epicardial (EPI) and endocardial (ENDO) left ventricular myocytes in the Goto-Kakizaki (GK) type 2 diabetic rat heart. Shortening and intracellular Ca2+ transients were measured by video edge detection and fluorescence photometry. Myocyte surface area was increased in EPI-GK and ENDO-GK compared to EPI-CON and ENDO-CON myocytes. Time to peak (TPK) shortening was prolonged in EPI-GK compared to EPI-CON and in ENDO-CON compared to EPI-CON myocytes. Time to half (THALF) relaxation of shortening was prolonged in EPI-GK compared to EPI-CON myocytes. TPK Ca2+ transient was prolonged in EPI-GK compared to EPI-CON myocytes. THALF decay of the Ca2+ transient was prolonged in EPI-CON compared to EPI-GK and in EPI-CON compared to ENDO-CON myocytes. Amplitude of shortening and the Ca2+ transient were unaltered in EPI-GK and ENDO-GK compared to their respective controls. Sarcoplasmic reticulum Ca2+ and myofilament sensitivity to Ca2+ were unaltered in EPI-GK and ENDO-GK compared to their respective controls. Regional differences in Ca2+ signaling in healthy and diabetic myocytes may account for variation in the dynamics of myocyte shortening. Further studies will be required to clarify the mechanisms underlying regional differences in the time course of shortening and the Ca2+ transient in EPI and ENDO myocytes from diabetic and control hearts.