Nava Pilar, Carbó Roxana, Guarner Verónica
Physiology Department, National Institute of Cardiology Ignacio Chávez, INCICH, Juan Badiano 1, Col. Sección XVI, Tlalpan 14080, México D.F.
Arch Cardiol Mex. 2003 Oct-Dec;73(4):253-60.
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.
雌激素对女性外周血管和冠状动脉疾病的保护作用已有充分文献记载；然而，糖尿病女性并不存在这种作用。雌激素通过非基因组机制降低张力发展，这些机制包括内皮细胞和平滑肌细胞中钙浓度的变化，以及内皮细胞中一氧化氮合酶（NOS）的调节。胰岛素增加内皮细胞释放内皮素-1（ET-1），调节平滑肌钙水平并增强股动脉和冠状动脉产生的力量。本文研究17β-雌二醇（E2β）是否调节胰岛素诱导的股动脉和冠状动脉收缩性变化。从雄性Wistar大鼠获取股动脉和冠状动脉，置于离体组织浴槽中进行体外研究，用不同溶液灌注，并测量对40 mmol/L KCl的收缩反应。胰岛素增加KCl诱导的动脉收缩。去除内皮后这种增加不存在。在有E2β存在时，我们观察到所产生张力呈剂量依赖性降低，去除内皮后这种效应消失。在有E2β存在时，胰岛素诱导的收缩显著降低。这些数据表明，E2β调节胰岛素对股动脉和冠状动脉血管收缩性的作用。
