© 1997 by European Society of Cardiology
Copyright © 1997, European Society of Cardiology
Intracellular calcium levels are unchanged in the diabetic heart
aCardiovascular Research Laboratory, Department of Pathology and Laboratory Medicine, Faculty of Medicine, The University of British Columbia, Vancouver, BC V6T 1Z3, Canada
bDivision of Pharmacology and Toxicology, Faculty of Pharmaceutical Sciences, The University of British Columbia, Vancouver, BC V6T 1Z3, Canada
* Corresponding author. Tel. +1 604 822-9373; Fax +1 604 822-8001.
Received 24 October 1996; accepted 9 January 1997
KEYWORDS Diabetes; Cardiomyopathy; Calcium, intracellular concentration; SR, calcium release
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1 Introduction |
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Diabetes mellitus has been associated with cardiac disease that has been suggested to occur secondary to atherosclerosis of the coronary arteries, macroangiopathy and autonomic neuropathy [1]. However, a cardiac disease particular to diabetes has also been demonstrated to occur in the absence of the above factors. This ‘diabetic cardiomyopathy’ that includes cardiomegaly, left ventricular dysfunction and clinically overt congestive heart failure has been strongly suggested by epidemiological, clinical and experimental studies [2–7]. The etiology of diabetic cardiomyopathy is complex and a number of factors have been suggested to be involved in the development of this disease state. These include: (a) changes in cardiac metabolism, (b) abnormal vascular sensitivity and reactivity to various ligands, (c) increased stiffness of the ventricular wall associated with perivascular thickening of basement membrane and interstitial accumulation of glycoprotein and insoluble collagen, and (d) abnormalities of various proteins which control ion movements, specifically intracellular calcium
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2 [Ca2+]i mobilization in ventricular myocytes |
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3 Intracellular Ca2+ in the diabetic heart |
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4 [Ca2+] mobilization in the diabetic heart |
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4.1 Sarcolemmal Ca2+ channels and Ca2+ and K+ currents in diabetic cardiomyocytes
4.2 Na–Ca exchange activity in SL of diabetic myocardium
4.3 SR Ca2+-ATPase in diabetic cardiomyocytes
4.3.1 Rapid-cooling and caffeine contractures
4.3.2 Caffeine-induced calcium transients in quiescent myocytes
4.4 Mitochondrial function in diabetic hearts
4.5 Myofilaments and Ca2+ sensitivity in diabetic cardiomyocytes
4.6 [Ca2+]i responses to β-adrenergic stimulation
4.7 [Ca2+]i responses to different pharmacological agents
4.7.1 Isoproterenol and 8-bromo-cAMP
4.7.2 Ouabain
4.7.3 KCl and ATP
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5 Summary |
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