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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Increased tail artery vascular responsiveness to angiotensin II in cold-treated rats.
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Increased tail artery vascular responsiveness to angiotensin II in cold-treated rats.

机译：在冷治疗的大鼠中尾动脉血管对血管紧张素II的反应性增加。

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Chronic exposure of rats to cold for 1-3 weeks results in a mild form of hypertension. The renin-angiotensin system (RAS) has been implicated in this model of cold-induced hypertension. Previously we have characterized the vascular responsiveness in cold-acclimated animals, using aortic tissue, and recent studies have focused on the thermoregulatory responses of angiotensin II (AngII), utilizing the tail artery of the rat. Therefore in the current study we evaluated the vascular responsiveness of cold-treated rats to AngII in both aorta and tail artery at 2 and 4 weeks of cold exposure (5+/-2 degrees C). Systolic blood pressures were significantly elevated in cold-treated animals compared with control animals at both 2 and 4 weeks of cold exposure. At both of these time points body weights were reduced and ventricular weights were increased in cold-treated animals. After 2 weeks of cold exposure the vascular responsiveness of the aorta to AngII was significantly lower than that of controls. This vascular responsiveness to AngII was elevated and returned to control levels after 5 weeks of cold exposure. However, this pattern was not observed in the tail artery. The vascular responsiveness of tail artery rings from cold-treated rats to AngII was significantly greater than that of control animals during both 2 and 5 weeks of exposure to cold. The vascular contractile responses of both the aorta and tail artery to KCI in the cold-treated animals was not different from that of the control animals maintained at ambient room temperature, suggesting that the vascular smooth muscle contractile components were not altered by the cold exposure. Thus, the in vitro vascular reactivity to the receptor-mediated vasoconstrictor AngII was decreased in the sparsely innervated aorta and increased in the more densely innervated tail artery of the cold-treated animals when compared with controls. These results suggest that the increased responsiveness of AngII on the smooth muscle of the tail artery may play a role in adaptation to the cold and the maintenance of cold-induced hypertension.
机译：将大鼠长期暴露于寒冷中1-3周会导致轻度高血压。肾素-血管紧张素系统（RAS）已牵涉到这种冷诱发的高血压模型中。以前，我们已经利用主动脉组织表征了冷适应动物的血管反应性，最近的研究集中在利用大鼠尾动脉的血管紧张素II（AngII）的温度调节反应上。因此，在本研究中，我们评估了冷暴露（5 +/- 2摄氏度）第2和第4周时，冷处理大鼠对主动脉和尾动脉中AngII的血管反应性。与对照组动物相比，在冷暴露2周和4周时，冷处理动物的收缩压均显着升高。在这两个时间点上，经过冷处理的动物的体重均减少，心室重量增加。冷暴露2周后，主动脉对AngII的血管反应显着低于对照组。冷暴露5周后，对AngII的这种血管反应性升高并恢复到对照水平。但是，这种模式在尾动脉中未观察到。在暴露于寒冷的2周和5周期间，来自冷处理大鼠的尾动脉环对AngII的血管反应性显着高于对照动物。在冷处理动物中，主动脉和尾动脉对KCI的血管收缩反应与保持在室温下的对照动物没有什么不同，这表明冷暴露不会改变血管平滑肌的收缩成分。因此，与对照相比，在冷处理的动物的稀疏支配的主动脉中，对受体介导的血管收缩剂AngII的体外血管反应性降低，而在较致密的支配的尾动脉中，其体外血管反应性升高。这些结果表明，AngII对尾动脉平滑肌的响应性增强可能在适应寒冷和维持寒冷诱发的高血压中起作用。

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