Simansky K J, Smith G P
Peptides. 1983 Mar-Apr;4(2):159-63. doi: 10.1016/0196-9781(83)90107-9.
Rats were tested two or three days after bilateral abdominal vagotomy or a laparotomy control procedure for their drinking responses to subcutaneous (1 mg-kg-1) or intracerebroventricular (100 ng) injections of angiotensin II. Vagotomy delayed the initiation of drinking and decreased 60-min water intake after subcutaneous, but not after intracerebroventricular, angiotensin II. This is the shortest postoperative interval in which the decrease in drinking after systemic injection of angiotensin II by abdominal vagotomy has been observed. The failure of vagotomy to decrease the response to intracerebroventricular angiotensin II demonstrates that the deficit after subcutaneous injection was not a nonspecific effect of recent vagotomy. These results, therefore, suggest that the abdominal vagus is necessary for normal drinking in response to circulating angiotensin II. Furthermore, the selective and acute onset of the deficit is consistent with the loss of a specific, rather than tonic facilitatory, vagal mechanism for drinking after elevation of circulating angiotensin II levels. Finally, the results imply that the physiological mechanisms which mediate the drinking responses to central and peripheral angiotensin are not identical.
在双侧腹部迷走神经切断术或剖腹手术对照程序后的两到三天，对大鼠进行测试，观察它们对皮下注射（1毫克/千克）或脑室内注射（100纳克）血管紧张素II的饮水反应。迷走神经切断术延迟了饮水的开始，并减少了皮下注射血管紧张素II后60分钟的饮水量，但脑室内注射血管紧张素II后未出现这种情况。这是观察到腹部迷走神经切断术导致全身注射血管紧张素II后饮水减少的最短术后间隔时间。迷走神经切断术未能降低对脑室内血管紧张素II的反应，这表明皮下注射后的缺陷不是近期迷走神经切断术的非特异性效应。因此，这些结果表明，腹部迷走神经对于正常情况下对循环血管紧张素II的饮水反应是必需的。此外，缺陷的选择性和急性发作与循环血管紧张素II水平升高后丧失特定的而非紧张性促进的迷走神经饮水机制一致。最后，结果表明介导对中枢和外周血管紧张素饮水反应的生理机制并不相同。
