Summy-Long J Y, Keil L C, Deen K, Severs W B
J Pharmacol Exp Ther. 1981 Jun;217(3):630-7.
In rats, intracerebroventricular (i.v.t.) administration of endogenous opioid peptides inhibited angiotensin II-stimulated increase in plasma vasopressin concentration and drinking behavior. Naloxone and naltrexone were used to evaluate the effect of opiate receptor blockade on angiotensin drinking behavior. Both antagonists reduced the amount of water consumed and number of animals drinking in response to angiotensin II (i.v.t.). The time to onset of drinking was unaffected. Leucine5-enkephalin inhibition of angiotensin-stimulated release of vasopressin was also studied. Changes in plasma vasopressin concentration with time (5, 45, 90, 150 and 300 sec) were measured after a single i.v.t. injection of angiotensin II (50 ng), with and without pretreatment with leucine5-enkephalin (100 microgram i.v.t.). Vasopressin was measured by radioimmunoassay. The onset of vasopressin release occurred 5 to 45 sec after angiotensin, reaching peak response between 45 to 90 sec. Leucine5-enkephalin did not affect the onset but reduced the peak response to angiotensin (P less than .05). Saralasin, i.v.t., abolished angiotensin-stimulated increase in plasma vasopressin concentration and prevented the residual, but significant, increase in plasma vasopressin concentration in angiotensin-treated rats given enkephalin. It is concluded that angiotensin stimulates release of vasopressin by interaction with specific, saralasin-sensitive, receptors; leucine5-enkephalin inhibits angiotensin release of vasopressin; and an endogenously synthesized opiate ligand(s) may affect angiotensin drinking behavior.
在大鼠中，脑室内（i.v.t.）注射内源性阿片肽可抑制血管紧张素II刺激引起的血浆血管加压素浓度升高和饮水行为。纳洛酮和纳曲酮用于评估阿片受体阻断对血管紧张素诱导的饮水行为的影响。两种拮抗剂均减少了血管紧张素II（i.v.t.）刺激下的饮水量和饮水动物数量。饮水开始时间未受影响。还研究了亮氨酸脑啡肽对血管紧张素刺激的血管加压素释放的抑制作用。在单次i.v.t.注射血管紧张素II（50 ng）后，分别在有和没有预先注射亮氨酸脑啡肽（100微克i.v.t.）的情况下，测量了血浆血管加压素浓度随时间（5、45、90、150和300秒）的变化。采用放射免疫分析法测定血管加压素。血管加压素释放在血管紧张素注射后5至45秒开始，在45至90秒之间达到峰值反应。亮氨酸脑啡肽不影响起始时间，但降低了对血管紧张素的峰值反应（P小于0.05）。i.v.t.注射沙拉新消除了血管紧张素刺激引起的血浆血管加压素浓度升高，并防止了在给予脑啡肽的血管紧张素处理大鼠中血浆血管加压素浓度残留但显著的升高。得出的结论是，血管紧张素通过与特定的、对沙拉新敏感的受体相互作用来刺激血管加压素释放；亮氨酸脑啡肽抑制血管紧张素诱导的血管加压素释放；并且内源性合成的阿片配体可能影响血管紧张素诱导的饮水行为。
