Mathai M L, Hübschle T, McKinley M J
Howard Florey Institute, University of Melbourne, Parkville, Victoria 3052, Australia.
Am J Physiol Regul Integr Comp Physiol. 2000 Nov;279(5):R1821-6. doi: 10.1152/ajpregu.2000.279.5.R1821.
The effect of central angiotensin AT(1) receptor blockade on thermoregulation and water intake after heat exposure was investigated. Rats were placed in a chamber heated to 39 +/- 1 degrees C for 60 min and then returned to their normal cage (at 22 degrees C), and water intake was measured for 120 min. Artificial cerebrospinal fluid (5 microl) was injected intracerebroventricularly 60 min before heat exposure in five control rats. Colonic temperature increased from 37.22 +/- 0.21 to 40.68 +/- 0.31 degrees C after 60 min. In six rats injected intracerebroventricularly with 10 microg of the AT(1) antagonist losartan, colonic temperature increased from 37.41 +/- 0.27 to 41.72 +/- 0.28 degrees C after 60 min. This increase was significantly greater than controls (P < 0.03). Losartan-treated rats drank 1.1 +/- 0.4 ml of water compared with 5.9 +/- 0.77 ml (P < 0.002) drank by control animals, despite a similar body weight loss in the two groups. Central losartan did not inhibit the drinking response to intracerebroventricular carbachol in heated rats, suggesting that losartan treatment did not nonspecifically depress behavior. We conclude that central angiotensinergic mechanisms have a role in both thermoregulatory cooling in response to heat exposure and also the ensuing water intake.
研究了中枢血管紧张素AT(1)受体阻断对热暴露后体温调节和水摄入的影响。将大鼠置于加热至39±1℃的实验箱中60分钟，然后放回正常饲养笼（22℃），并测量120分钟内的水摄入量。在五只对照大鼠热暴露前60分钟，脑室内注射人工脑脊液（5微升）。60分钟后，结肠温度从37.22±0.21℃升高至40.68±0.31℃。在六只脑室内注射10微克AT(1)拮抗剂氯沙坦的大鼠中，60分钟后结肠温度从37.41±0.27℃升高至41.72±0.28℃。这种升高显著大于对照组（P<0.03）。尽管两组体重减轻相似，但氯沙坦处理的大鼠饮水1.1±0.4毫升，而对照动物饮水5.9±0.77毫升（P<0.002）。中枢给予氯沙坦并不抑制热暴露大鼠对脑室内注射卡巴胆碱的饮水反应，这表明氯沙坦处理并非非特异性地抑制行为。我们得出结论，中枢血管紧张素能机制在热暴露后的体温调节性散热以及随后的水摄入中均起作用。
