Voltage dependence of the Ca2+ transient in endocardial and epicardial myocytes from the left ventricle of Goto Kakizaki type 2 diabetic rats
Author | Al Kury, Lina |
Author | Sydorenko, Vadym |
Author | Smail, Manal M. A. |
Author | Qureshi, Muhammad Anwar |
Author | Shmygol, Anatoliy |
Author | Oz, Murat |
Author | Singh, Jaipaul |
Author | Howarth, Frank Christopher |
Available date | 2020-03-03T06:19:36Z |
Publication Date | 2018 |
Publication Name | Molecular and Cellular Biochemistry |
Resource | Scopus |
ISSN | 3008177 |
Abstract | Diabetes mellitus is a major global health disorder and, currently, over 450 million people have diabetes with 90% suffering from type 2 diabetes. Left untreated, diabetes may lead to cardiovascular diseases which are a leading cause of death in diabetic patients. Calcium is the trigger and regulator of cardiac muscle contraction and derangement in cellular Ca2+ homeostasis, which can result in heart failure and sudden cardiac death. It is of paramount importance to investigate the regional involvement of Ca2+ in diabetes-induced cardiomyopathy. Therefore, the aim of this study was to investigate the voltage dependence of the Ca2+ transients in endocardial (ENDO) and epicardial (EPI) myocytes from the left ventricle of the Goto–Kakizaki (GK) rats, an experimental model of type 2 diabetes mellitus. Simultaneous measurement of L-type Ca2+ currents and Ca2+ transients was performed by whole-cell patch clamp techniques. GK rats displayed significantly increased heart weight, heart weight/body weight ratio, and non-fasting and fasting blood glucose compared to controls (CON). Although the voltage dependence of L-type Ca2+ current was unaltered, the voltage dependence of the Ca2+ transients was reduced to similar extents in EPI–GK and ENDO–GK compared to EPI–CON and ENDO–CON myocytes. TPK L-type Ca2+ current and Ca2+ transient were unaltered. THALF decay of L-type Ca2+ current was unaltered; however, THALF decay of the Ca2+ transient was shortened in ENDO and EPI myocytes from GK compared to CON rat hearts. In conclusion, the amplitude of L-type Ca2+ current was unaltered; however, the voltage dependence of the Ca2+ transient was reduced to similar extents in EPI and ENDO myocytes from GK rats compared to their respective controls, suggesting the possibility of dysfunctional sarcoplasmic reticulum Ca2+ transport in the GK diabetic rat hearts. |
Sponsor | This work has been supported by a grant from the College of Medicine & Health Sciences, United Arab Emirates University, Al Ain; Sheikh Hamdan Bin Rashid Al Maktoum Award, Dubai; Zayed University, Abu Dhabi; and funding from the Al Ain Equestrian, Shooting and Golf Club. |
Language | en |
Publisher | Springer New York LLC |
Subject | Ca2+ transient Diabetes Endocardial myocytes Epicardial myocytes Goto?Kakizaki rat L-type Ca2+ current Rat heart Ventricle |
Type | Article |
Pagination | 25 - 33 |
Issue Number | 2-Jan |
Volume Number | 446 |
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