Diabetes mellitus produces functional, biochemical and morphological myocardial abnormalities independent of
coronary atherosclerosis and
hypertension. Although tight
glycemic control decreases the risk of
heart failure in patients with diabetes, the effects of different diabetic treatment regimens on
heart failure have yet to be determined and remain subject to further investigation.Evidence suggests that
reactive oxygen species play an important role in the development of
diabetic cardiomyopathy, and
antioxidants have been used to reduce
cardiomyopathy in patients with diabetes. Therefore, the present study examines the treatment of
streptozotocin-induced diabetic rats with
sodium selenite (5 mumol/kg/day, intraperitoneally). The results showed that
sodium selenite treatment could restore the altered mechanical and electrical activities of diabetic rat hearts. The results also demonstrate that the beneficial effects of this treatment on diabetic rat heart dysfunction appear to be due to the restoration of diminished K(+) currents; the restoration of increased intracellular Ca(2+) concentrations in diabetes; and all these beneficial effects are partially related to the restoration of the cell
glutathione redox cycle.It has been hypothesized that the
angiotensin II (Ang II) signalling pathway may also play a role in the development of
diabetic cardiomyopathy. It is the ability of Ang II to produce
reactive oxygen species and the involvement of these molecules in signal transduction that are the hallmark of Ang II activation. Although action potential prolongation and diminished K(+) currents were reversed by
angiotensin receptor type I (AT(1)) blockers in diabetic rat heart, their effects on Ca(2+) homeostasis in diabetic cardiomyocytes are not yet clear. Thus, the effects of AT(1) blocker treatment (
candesartan cilexetil) on cardiac Ca(2+) metabolism, and on the contractile state and electrical activity of papillary muscle in diabetic rats were examined. It was shown that treatment with an AT(1) blocker restored the altered kinetics of Ca2+ transients in cardiomyocytes and the contractile activity in papillary muscle strips from diabetic rats. Thus, Ang II receptor blockade protects the heart from the development of cellular alterations that are typically related to diabetes.