Fregly M J, Shechtman O, Rowland N E
Department of Physiology, University of Florida, College of Medicine, Gainesville 32610, USA.
Proc Soc Exp Biol Med. 1995 May;209(1):54-9. doi: 10.3181/00379727-209-43877.
Subcutaneous administration of angiotensin II (Ang II) to rats exposed chronically to 5 degrees C induced an increased drinking response compared with that of warm-acclimated controls. The exaggerated drinking response was also observed when graded doses of Ang II were administered into the lateral cerebroventricle (icv) of chronically cold-exposed rats. A maximal drinking response occurred in cold-treated, but not in control, rats when the lowest dose of Ang II (1.6 ng/rat) was administered icv. Thus, it is clear that the dipsogenic responsiveness to either centrally or peripherally administered Ang II is increased by chronic exposure to cold. To assess whether the increased responsiveness was retained after removal from cold, graded doses of Ang II were administered to rats removed from cold to a thermoneutral environment. The results again showed a maximal responsiveness to the lowest dose of Ang II administered (25 micrograms/kg, sc) to cold-treated rats that had either just been removed from cold or removed from cold 2 hr prior to treatment. Cold-exposed rats had an ED50 for Ang II-induced drinking that was about half that of their warm-acclimated controls. To assess how long the cold-induced increase in dipsogenic responsiveness to Ang II lasted after return to a thermoneutral temperature, rats were removed from cold for 24, 48, or 60 hr and then administered graded doses of Ang II (25, 50, or 100 micrograms/kg, sc). The results suggest that between 46 and 52 hr after removal from cold, the cold-induced increase in dipsogenic responsiveness to Ang II returned to the level of the controls. Hence, the physiological changes in the dipsogenic mechanism induced by exposure to cold are not immediately reversible when the rats are returned to a thermoneutral ambient temperature.
与适应温暖环境的对照组相比，对长期暴露于5摄氏度环境的大鼠皮下注射血管紧张素II（Ang II）会引起饮水反应增加。当向长期暴露于寒冷环境的大鼠侧脑室（icv）注射不同剂量的Ang II时，也观察到了夸张的饮水反应。当向冷处理大鼠而非对照大鼠icv注射最低剂量的Ang II（1.6 ng/只）时，出现了最大饮水反应。因此，很明显，长期暴露于寒冷环境会增加对中枢或外周给予的Ang II的致渴反应性。为了评估从寒冷环境中移出后这种增加的反应性是否仍然存在，将不同剂量的Ang II给予从寒冷环境转移到热中性环境的大鼠。结果再次显示，对刚从寒冷环境中移出或在给药前2小时从寒冷环境中移出的冷处理大鼠，给予最低剂量的Ang II（25微克/千克，皮下注射）时出现最大反应性。暴露于寒冷环境的大鼠对Ang II诱导饮水的半数有效剂量（ED50）约为适应温暖环境对照组的一半。为了评估回到热中性温度后，寒冷诱导的对Ang II致渴反应性增加持续多长时间，将大鼠从寒冷环境中移出24、48或60小时，然后给予不同剂量的Ang II（25、50或100微克/千克，皮下注射）。结果表明，从寒冷环境中移出后46至52小时之间，寒冷诱导的对Ang II致渴反应性增加恢复到对照组水平。因此，当大鼠回到热中性环境温度时，暴露于寒冷环境引起的致渴机制的生理变化不会立即逆转。
