Kau M M, Tsai L M, Hsieh P S, Ko G S, Huang W C
National Taipei College of Nursing, Department of Physiology and Biophysics, Taiwan.
Chin J Physiol. 1994;37(1):37-42.
Our previous studies have shown that sustained hyperinsulinemia increases blood pressure in rats. The precise mechanism is still unclear. The present study was conducted to assess if hyperinsulinemia could interact with angiotensin II and other pressor stimuli to increase blood pressure in renovascular hypertensive rats. Intact and uninephrectomized Sprague-Dawley rats with unilateral renal arterial constriction (2-kidney, 1 clip and 1-kidney, 1 clip Goldblatt rats) were administered insulin (3 mU/kg/min) for 6-12 weeks. The clipped rats without insulin infusion and normal rats served as controls. Changes in blood pressure were measured by tailcuff method without preheating. Results showed that either sustained infusion of insulin or renal arterial clipping alone in normal rats significantly increased the blood pressure. Superimposed infusion of insulin for 6-7 weeks into rats with unilateral renal artery constriction in either 2-kidney or 1-kidney model did not accelerate nor exacerbate the development of hypertension. There were no significant differences in body weight and plasma levels of glucose, triglycerides, sodium and potassium between 2-kidney, 1 clip Goldblatt hypertensive rats with and without insulin infusion. These data suggest that chronic hyperinsulinemia and angiotensin II do not act synergistically to increase the blood pressure in rats.
我们之前的研究表明，持续性高胰岛素血症会使大鼠血压升高。确切机制仍不清楚。本研究旨在评估高胰岛素血症是否会与血管紧张素II及其他升压刺激相互作用，从而使肾血管性高血压大鼠的血压升高。对完整的和单侧肾切除的Sprague-Dawley大鼠进行单侧肾动脉缩窄（双肾单夹和单肾单夹Goldblatt大鼠），给予胰岛素（3 mU/kg/分钟），持续6至12周。未输注胰岛素的夹闭大鼠和正常大鼠作为对照。采用不预热的尾套法测量血压变化。结果显示，正常大鼠单独持续输注胰岛素或单独进行肾动脉夹闭均可显著升高血压。在双肾或单肾模型中，对单侧肾动脉缩窄的大鼠叠加输注胰岛素6至7周，既不会加速也不会加剧高血压的发展。输注胰岛素和未输注胰岛素的双肾单夹Goldblatt高血压大鼠在体重以及血浆葡萄糖、甘油三酯、钠和钾水平方面均无显著差异。这些数据表明，慢性高胰岛素血症和血管紧张素II不会协同作用使大鼠血压升高。
