Van de Kar L D, Lorens S A, Urban J H, Richardson K D, Paris J, Bethea C L
Brain Res. 1985 Oct 21;345(2):257-63. doi: 10.1016/0006-8993(85)91001-7.
Stress-induced renin and prolactin secretion was investigated using a conditioned emotional response paradigm. Three minutes after placement in a chamber the rats received an electric shock to their feet via the grid floor, then were immediately returned to their home cage. This procedure was repeated for 3 consecutive days. On the fourth day, instead of receiving an electric shock, they were removed after 3 min and sacrificed by decapitation. Control rats were treated identically with the exception that shock was not administered at any time. There was a significant increase in plasma renin activity and prolactin level in the stressed rats. The administration of the antianxiety drugs chlordiazepoxide (10 mg/kg i.p.) or midazolam (0.125-2 mg/kg i.p.) blocked the stress-induced increase in prolactin levels but not the stress-induced rise in plasma renin activity. Administration of the beta-blocker propranolol (1 mg/kg i.p.) inhibited, but did not completely block, stress-induced rise in plasma-renin activity and had no effect on stress-induced prolactin secretion. The opiate antagonist naloxone (0.1-10 mg/kg i.p.) and the acetylcholinesterase inhibitor diisopropyl fluorophosphate (0.5 mg/kg i.p.) did not block stress-induced renin or prolactin secretion. It is concluded that stress-induced prolactin secretion is regulated by a benzodiazepine-mediated mechanism and that stress-induced renin but not prolactin secretion is mediated in part via beta-receptors.
采用条件性情绪反应范式研究应激诱导的肾素和催乳素分泌。将大鼠放入实验箱3分钟后,通过网格地板对其足部施加电击,然后立即放回其笼舍。此过程连续重复3天。在第4天,大鼠在3分钟后不接受电击,而是取出并断头处死。对照大鼠的处理方式相同,只是在任何时候都不施加电击。应激大鼠的血浆肾素活性和催乳素水平显著升高。给予抗焦虑药物氯氮卓(10mg/kg腹腔注射)或咪达唑仑(0.125 - 2mg/kg腹腔注射)可阻断应激诱导的催乳素水平升高,但不能阻断应激诱导的血浆肾素活性升高。给予β受体阻滞剂普萘洛尔(1mg/kg腹腔注射)可抑制但不能完全阻断应激诱导的血浆肾素活性升高,且对应激诱导的催乳素分泌无影响。阿片拮抗剂纳洛酮(0.1 - 10mg/kg腹腔注射)和乙酰胆碱酯酶抑制剂二异丙基氟磷酸酯(0.5mg/kg腹腔注射)不能阻断应激诱导的肾素或催乳素分泌。结论是,应激诱导的催乳素分泌受苯二氮卓介导的机制调节,应激诱导的肾素而非催乳素分泌部分通过β受体介导。