Shido O, Kifune A, Nagasaka T
Jpn J Physiol. 1985;35(2):301-9. doi: 10.2170/jjphysiol.35.301.
The mechanisms of the hypothermic effect of angiotensin II (AII) injected into the lateral ventricle were investigated in unanesthetized rats at an ambient temperature of 18 degrees C. Mean blood pressure (BP), heart rate (HR), metabolic rate (M), colonic temperature (Tcol), and temperatures of the interscapular brown adipose tissue (TBAT), and the tail skin (Tsk) were continuously monitored. AII at a dose of 5 micrograms produced a sharp and marked elevation in BP accompanied by bradycardia, and a decrease of M and Tco1 in the sinoaortic baroreceptor intact rats. The difference between TBAT and Tcol decreased significantly, which suggests a suppression of nonshivering thermogenesis of the BAT. Tsk was not changed by the AII injection. After sinoaortic denervation, however, the decrease in Tcol and M with AII injection was significantly reduced despite a marked elevation in BP. In addition, intravenous arginine-vasopressin antagonist pretreatment suppressed the elevation in BP and the decrease in HR, Tcol, and M after AII injection. From these results, it is concluded that the hypothermia which occurred after AII injection into the lateral ventricle can be largely attributed to the baroreflexive suppression of M, and to some extent to the direct effect on the thermoregulatory center in rats.
在环境温度为18摄氏度的未麻醉大鼠中，研究了注入侧脑室的血管紧张素II（AII）产生低温效应的机制。持续监测平均血压（BP）、心率（HR）、代谢率（M）、结肠温度（Tcol）、肩胛间棕色脂肪组织温度（TBAT）和尾皮肤温度（Tsk）。剂量为5微克的AII可使主动脉弓和颈动脉窦压力感受器完整的大鼠血压急剧显著升高，伴有心动过缓，同时M和Tcol降低。TBAT与Tcol之间的差异显著减小，这表明棕色脂肪组织的非寒战产热受到抑制。注射AII后Tsk未发生变化。然而，在主动脉弓和颈动脉窦去神经支配后，尽管血压显著升高，但注射AII后Tcol和M的降低明显减少。此外，静脉注射精氨酸血管加压素拮抗剂预处理可抑制注射AII后血压的升高以及HR、Tcol和M的降低。从这些结果可以得出结论，注入侧脑室的AII后出现的体温过低在很大程度上可归因于压力反射对M的抑制，并且在一定程度上归因于对大鼠体温调节中枢的直接作用。
