Cell shortening and calcium dynamics in epicardial and endocardial myocytes from the left ventricle of the Goto-Kakizaki 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.

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