感觉神经损伤性盐敏感性高血压大鼠新模型的建立及其细胞内游离钙的变化

The establishment of a novel salt-sensitive hypertensive model induced by sensory denervation and the change of its intracellular free Ca^(2+)

目的 建立一种新的感觉神经损伤性盐敏感性高血压大鼠模型 ,并探讨该模型细胞内游离钙 ([Ca2 + ]i)的变化。方法 新生Wistar大鼠皮下注射辣椒辣素 (5 0mg/kg) ,对照组则皮下注射对照液 ,哺乳期后挑选出雄性大鼠分成 4组分别给予含盐不同的饮食 4周 ,检测鼠尾收缩压、体重、淋巴细胞 [Ca2 + ]i 和 2 4h尿量、饮水量、尿钠、尿钾。结果 辣椒辣素处理的新生大鼠在高盐饮食时鼠尾收缩压、淋巴细胞 [Ca2 + ]i 明显增高 ,肾排钠和水功能降低。结论 新生大鼠辣椒辣素敏感性感觉神经损伤可使大鼠在盐负荷时血压显著而持久地升高、细胞 [Ca2 + ]i 明显升高及肾排钠和水功能受损。

Objectives To establish a salt sensitive hypertensive rat model induced by sensory denervation and to observe the change of its intracellular free Ca 2+ concentration ([Ca 2+ ] i). Methods Newborn Wistar rats were given 50 mg/kg capsaicin subcutaneously on the 1st and 2nd day of life. Control rats were treated with vehicle. After weanling period, male rats were divided into 4 gruops and fed different salt diets for 4 weeks. Tail cuff systolic blood pressure, body weight, intralymphocytes [Ca 2+ ] i, 24 hour urinary volume,water intake, urinary Na + and K + concentrations were examined. Results Neonatal treatment with capsaicin led to the elevation of blood pressure and intralymphocytes [Ca 2+ ] i in rats fed a high salt diet. Neonatal treatment with capsaicin impaired proportional urine excretion and urine sodium excretion when rats were loaded with salt. Conclusions This study provides that neonatal degeneration of capsaicin sensitive sensory nerves causes the rat to respond to a salt load with a significant and sustained rise in blood pressure and significant rise in intralymphocytes [Ca 2+ ] i. Our data also suggest that neonatal capsaicin treatment may impair renal sodium and water excretions in response to high sodium intake.