Regulation of intracellular Ca2+ in the heart during diabetes.
Cardiovascular disease is a significant medical problem. The diabetic population is even more susceptible to cardiovascular complications and heart failure than non-diabetic patients. Atherosclerotic complications, a neuropathy and microvascular lesions have all been implicated causally in the accelerated cardiovascular disease during diabetes. However, one mechanism which may participate in the abnormalities in heart performance demonstrated during diabetes and may also contribute to heart failure in the diabetic is a derangement in the capacity of the myocardial cell to regulate its [Ca2+]. The purpose of this treatise is to identify the current controversies and conclusions available regarding the specific defects in Ca2+ flux thought to contribute to these cardiac defects during diabetes mellitus.
Pierce
G N
GN
Institute of Cardiovascular Sciences, St. Boniface General Hospital Research Centre, Winnipeg, MB, Canada. pierce@sbrc.umanitoba.ca
Russell
J C
JC
D000818:Animals; D002118:Calcium / Q000378:metabolism*; D003285:Contractile Proteins / Q000378:metabolism; D048909:Diabetes Complications; D003920:Diabetes Mellitus / Q000378:metabolism* / Q000503:physiopathology; D006801:Humans; D007424:Intracellular Fluid / Q000378:metabolism*; D009200:Myocardial Contraction; D017202:Myocardial Ischemia / Q000150:complications / Q000378:metabolism; D009206:Myocardium / Q000378:metabolism*; D051381:Rats
D003285:Contractile Proteins; D002118:Calcium