17 beta-estradiol modulates effects of insulin-induced changes in vascular contractility.

The protective role of estrogens against peripheral vascular and coronary disease in women is well documented; however, it is not present in diabetic women. Estrogens reduce tension development through non-genomic mechanisms that include changes in calcium concentrations in endothelial and smooth muscle cells, and regulation of nitric oxide synthase (NOS) in endothelial cells. Insulin increases endothelin-1 (ET-1) release from endothelial cells modulating smooth muscle calcium levels and elevating force generated by femoral and coronary arteries. This paper examines whether 17 beta-estradiol (E2 beta) modulates changes in femoral and coronary artery contractility induced by insulin. Femoral and coronary arteries were obtained from male Wistar rats, placed in isolated tissue baths for in vitro studies, perfused with different solutions, and the contractile response to KCl 40 mmol/L was measured. Insulin increased arterial contraction induced by KCl. This increase was not present when the endothelium was removed. In the presence of E2 beta, we observed a dose dependent reduction in the tension developed and this effect disappeared when the endothelium was removed. The insulin-induced contraction was significantly reduced in presence of E2 beta. These data indicate that the effect of insulin on femoral and coronary vascular contractility is modulated by E2 beta.