Summy-Long J Y, Keil L C, Sells G, Kirby A, Chee O, Severs W B
Am J Physiol. 1983 Apr;244(4):R522-9. doi: 10.1152/ajpregu.1983.244.4.R522.
The effect of leucine5-enkephalin (Leu-enkephalin) administered into the lateral (LV) or fourth (4V) cerebroventricle on angiotensin II (ANG II)-stimulated increase in blood pressure, plasma vasopressin concentration ([AVP]), and drinking behavior was determined in conscious rats. Leu-enkephalin (20, 50, or 100 micrograms) was injected into the LV (5 microliters) or 4V (2 microliters) less than or equal to 15 s before ANG II (50 or 500 ng, LV). LV and 4V administration of Leu-enkephalin (100 or 50 micrograms) significantly (P less than 0.05) delayed the drinking onset, decreased the number of animals drinking, and reduced the volume consumed (100 micrograms, 30 min) in response to ANG II (50 ng). ANG II-stimulated increases in plasma [AVP] and blood pressure were inhibited by 50 or 100 micrograms, respectively, of Leu-enkephalin administered into LV but not 4V. Decreased motor activity occurred after Leu-enkephalin (100 micrograms) administration into LV and 4V, whereas head shakes were more consistent after the former. Fast green dye administered into 4V did not reach anterior periaqueductal, third, or lateral cerebroventricular sites. Thus opioid peptide receptors inhibiting ANG II-stimulated drinking, vasopressin release, and pressor response are postulated to be in brain structures accessible from lateral or third cerebroventricles. Opiate receptors inhibitory to drinking are also reached from peri-4V sites.
在清醒大鼠中，研究了将亮氨酸脑啡肽（亮啡肽）注入侧脑室（LV）或第四脑室（4V）对血管紧张素II（ANG II）刺激引起的血压升高、血浆血管加压素浓度（[AVP]）及饮水行为的影响。在ANG II（50或500 ng，注入LV）注入前小于或等于15秒，将亮啡肽（20、50或100微克）注入LV（5微升）或4V（2微升）。LV和4V注入亮啡肽（100或50微克）显著（P<0.05）延迟了饮水开始时间，减少了饮水动物的数量，并减少了对ANG II（50 ng）的饮水消耗量（100微克，30分钟）。ANG II刺激引起的血浆[AVP]升高和血压升高分别被注入LV而非4V的50或100微克亮啡肽抑制。注入LV和4V的亮啡肽（100微克）后出现运动活动减少，而前者后摇头更常见。注入4V的固绿染料未到达导水管周围前部、第三脑室或侧脑室部位。因此，推测抑制ANG II刺激的饮水、血管加压素释放和升压反应的阿片肽受体位于可从侧脑室或第三脑室进入的脑结构中。对4V周围部位的刺激也可到达抑制饮水的阿片受体。
