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Effects of Streptozotocin‐Induced Diabetes on Contraction and Calcium Transport in Rat Ventricular Cardiomyocytes
Author(s) -
BRACKEN NICHOLAS,
HOWARTH FRANK C.,
SINGH JAIPAUL
Publication year - 2006
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1196/annals.1372.018
Subject(s) - medicine , endocrinology , contraction (grammar) , streptozotocin , diabetes mellitus , myocyte , calcium , caffeine , chemistry
Abstract: Cardiovascular diseases are the major cause of morbidity and mortality in diabetic patients. Contractile function of the heart is frequently compromised in the clinical setting and in experimental models of diabetes mellitus (DM). This article investigated the effect of streptozotocin (STZ)‐induced type 1 DM on contraction, L‐type calcium (Ca 2+ ) current (I Ca2+L ), and on cytosolic calcium concentrations [Ca 2+ ] i in ventricular myocytes of the rat heart. After 4–10 weeks of STZ treatment, blood glucose levels in diabetic animals were significantly ( P < 0.05) higher compared to age‐matched controls. Diabetic rats have significantly ( P < 0.05) reduced body, reduced heart weight, and reduced viability of ventricular myocytes compared to controls. The amplitude of I Ca2+L and amplitude of contraction were significantly reduced ( P < 0.05) at test potentials in the range –10 mV to +20 mV and –30 mV to +40 mV, respectively, in myocytes from diabetic animals compared to age‐matched controls. Moreover, there was a significant ( P < 0.05) delay in electrically stimulated and caffeine‐evoked time to half relaxation of the Ca 2+ transient in myocytes from diabetic animals compared to controls. A similar effect was obtained in myocytes treated with a combination of caffeine and nickel chloride (NiCl 2 ). It is concluded that the diabetes‐induced voltage‐dependent decrease in contraction is associated with reduced Ca 2+ channel activities and prolonged diastolic cytosolic Ca 2+ compared to age‐matched control. Taken together, the results suggest that Ca 2+ homeostasis is deranged during DM and this may be expressed at the level of the Na + /Ca 2+ exchanger.