The cardiovascular biology of hydrogen sulphide

Abstract

The present study examines the role of H2S in streptozotocin-injected rats; a well-established model of type-I diabetes mellitus. The biosynthesis of H2S in liver and pancreas was elevated in diabetic rats with concurrent increase in expression of H2S producing enzymes in these organs. Insulinoma (HIT-T15) cells exposed to NaHS (H2S donor) secreted less insulin. The mechanism of H2S-mediated attenuation of insulin release was found to involve K-ATP channel function. H2S synthesis was elevated in diabetic rat aorta homogenates and diabetic aortic rings were more sensitive to H2S-mediated vascular responses. The bolus (i.v.) administration of PAG, a CSE (H2S producing enzyme) inhibitor, to anaesthetized diabetic rats caused a modest but significant rise in mean arterial blood pressure (MAP) suggesting that H2S may contribute to diabetic vasculature and blood pressure aberrations. This study shows that H2S is most likely involved in insulin regulation and the pathogenesis of diabetes-related vascular complications.