Huang W C, Fang T C, Cheng J T
Graduate Institute of Medical Sciences, Tzu Chi College of Medicine, Hualien, Taiwan, Republic of China.
Hypertension. 1998 Aug;32(2):249-54. doi: 10.1161/01.hyp.32.2.249.
Experiments were performed to evaluate the role of the renal nerves in hyperinsulinemia-induced hypertension. Male Sprague-Dawley rats were made hyperinsulinemic by insulin infusion via osmotic minipumps implanted subcutaneously (3.0 mU/kg per minute for 6 weeks). Rats with vehicle infusion served as controls. Bilateral renal denervation was performed either at the beginning of or 4 weeks after insulin infusion. The systolic blood pressure was measured by the tail-cuff method twice a week. Food and water intake and urine flow were measured daily. The results showed that sustained insulin infusion significantly increased plasma insulin concentrations from 277.7+/-25.8 pmol/L to 609.9+/-22.2 and 696.7+/-23.0 pmol/L by the end of weeks 4 and 6, respectively (P<0.05). Systolic blood pressure was significantly increased from 135+/-3 to 157+/-3 and 159+/-2 mm Hg (P<0.05) at the corresponding time points. There was a significant increase in the plasma norepinephrine concentration after insulin infusion, whereas no significant changes in plasma triglyceride and glucose concentrations, water intake, urine flow, sodium excretion, sodium gain, and body weight gain were observed. Bilateral renal denervation depleted renal norepinephrine stores and prevented the development of hyperinsulinemia-induced hypertension. After hyperinsulinemia-induced hypertension had been fully established (from 134+/-2 to 157+/-2 mm Hg), bilateral renal denervation reversed the elevated systolic blood pressure to normotensive levels within 2 weeks. Transient denervated diuresis and natriuresis were observed. These results indicate that chronic hyperinsulinemia-induced hypertension requires the presence of intact renal nerves in rats.
进行实验以评估肾神经在高胰岛素血症诱导的高血压中的作用。通过皮下植入渗透微型泵输注胰岛素（3.0 mU/kg每分钟，持续6周）使雄性Sprague-Dawley大鼠产生高胰岛素血症。输注赋形剂的大鼠作为对照。在胰岛素输注开始时或4周后进行双侧肾去神经支配。每周两次通过尾套法测量收缩压。每天测量食物和水摄入量以及尿流量。结果显示，持续输注胰岛素使血浆胰岛素浓度在第4周和第6周末分别从277.7±25.8 pmol/L显著增加至609.9±22.2和696.7±23.0 pmol/L（P<0.05）。相应时间点的收缩压从135±3显著升高至157±3和159±2 mmHg（P<0.05）。胰岛素输注后血浆去甲肾上腺素浓度显著增加，而血浆甘油三酯和葡萄糖浓度、水摄入量、尿流量、钠排泄、钠潴留和体重增加均未观察到显著变化。双侧肾去神经支配耗尽了肾去甲肾上腺素储备，并阻止了高胰岛素血症诱导的高血压的发展。在高胰岛素血症诱导的高血压完全形成后（从134±2至157±2 mmHg），双侧肾去神经支配在2周内将升高的收缩压逆转至正常血压水平。观察到短暂的去神经利尿和利钠作用。这些结果表明，慢性高胰岛素血症诱导的高血压在大鼠中需要完整的肾神经存在。
