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Effects of Long‐term Administration of the KCa Channel Agonist SKA‐31 on Cardiovascular Function in the Type 2 Diabetic Goto‐Kakizaki Rat

It is now evident that small and intermediate‐conductance, Ca2+‐activated K+ channels (KCa 2.3 and KCa 3.1, respectively) expressed in vascular endothelium are intimately involved in agonist‐evoked vasodilation of small resistance arteries throughout the circulation. In myogenically active vasculature exhibiting endothelial dysfunction associated with Type 2 Diabetes (T2D), we have shown that pharmacologic “priming” of KCa 2.3 and KCa 3.1 channels with the KCa channel agonist SKA‐31can acutely improve agonist‐stimulated dilation in isolated, myogenically active resistance arteries and fluid flow in the intact coronary circulation of non‐obese T2D Goto‐Kakizaki (GK) rats. In the present study, we have hypothesized that chronic administration of SKA‐31 will mitigate the progression of cardiovascular complications associated with T2D‐associated endothelial dysfunction (e.g. hypertension, cardiac impairment, atherosclerosis). Experimentally, male GK rats were implanted with radio‐telemeters and treated with 10 mg/kg or 30 mg/kg SKA‐31 or drug vehicle by daily I.P. injection for up to 12 weeks. The main cardiovascular parameters being monitored in our study include: blood pressure and heart rate, in vivo cardiac function (echocardiography), plasma metabolic factors, and immune cell/plasma cytokine profiles. Ex vivo assessment of vascular function is carried out at the end of the treatment protocol. The purpose of this presentation is to describe the preliminary data gathered to date.