Contractile dysfunction is a frequently reported complication of diabetic cardiomyopathy and many of the defects observed in the clinical setting have also been reported in experimentally-induced diabetes. We have investigated the relationship between intracellular Ca2+ concentration and cell length during the relaxation phase of contraction in ventricular myocytes from streptozotocin (STZ) – induced diabetic rats. Cell length and intracellular Ca2+ concentration were measured simultaneously in electrically stimulated (1 Hz) myocytes loaded with fura-2 and maintained at 35-36 °C. The amplitude and time to peak shortening and Ca2+ transient were similar, however, the relaxation of contraction and the Ca2+ transient were significantly prolonged in myocytes from STZ-treated rats compared to controls. Myofilament Ca2+ sensitivity, which was assessed by plotting cell length against fura-2 fluorescence ratio during the relaxation phase of a contraction, was significantly increased in myocytes from STZtreated (9.23 ± 0.77 mm/fura-2 fluorescence unit) compare to controls (4.84 ± 0.78 mm/fura-2 fluorescence unit). The slower time course of relaxation of contraction and Ca2+ transient may be explained by defective sarcoplasmic reticulum Ca2+ uptake and to a lesser extent mechanisms of plasma membrane Ca2+ efflux including Na+/Ca2+ exchange and CaCa2+ATPase. In conclusion, the apparent increase in myofilament Ca2+ sensitivity may be attributed to slower cross-bridge cycling rate which in turn may be related to the alteration of expression of different myofilament myosin isoforms.

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