Modulation of hydrogen sulfide synthesis improve heart function and
endothelium-dependent vasorelaxation in diabetes
Abstract Diabetes dramatically increases the risk of cardiovascular complications. The endothelial dysfunction and diastolic heart dysfunction are associated with a decreasing level of hydrogen sulfide (H2S) and inhibition of the activity of endothelial NO-synthase in diabetes. The aim of work is to investigate the effect of modulation of hydrogen sulfide synthesis on heart functions and vasorelaxation in diabetes. The DL-propargylglycine and L-cysteine were administered intraperitoneally. H2S content in the heart tissue, markers of oxidative stress, iNOS and cNOS activities, endothelium-dependent vasorelaxation of the aortic rings, and heart function were studied. We demonstrate that our combination increased H2S syntheses by 13 times and cNOS activity by 5 times in the heart tissue of diabetic rats. Increasing NO and H2S production caused improving and restoration of endothelium-dependent relaxation of aorta, effective arterial elastance, and diastolic heart function in diabetic rats. The endothelium-dependent relaxation increased by 2.4 times; effective arterial elastance decreased by 47%. The end-diastolic myocardial stiffness decreased by 2.2 times. Thus, modulation of hydrogen sulfide synthesis leads to increased activity cNOS by 5 times in the cardiovascular system. Increasing NO and H2S production restored endothelium-dependent relaxation of aorta and improved heart function in diabetes.