Naloxone effects on plasma vasopressin and oxytocin concentrations elevated by histamine, nicotine, isoproterenol and an acute increase in [NaCl] in cerebrospinal fluid.
Naloxone effects on plasma vasopressin and oxytocin concentrations elevated by histamine, nicotine, isoproterenol and an acute increase in [NaCl] in cerebrospinal fluid.
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纳洛酮对因组胺、尼古丁、异丙肾上腺素和脑脊液中[NaCl]急剧增加而升高的血浆加压素和催产素浓度的影响。
DOI：
10.1159/000124639
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发表时间：
1986
影响因子：
4.1
通讯作者：
Rosella-Dampman,LM
中科院分区：
文献类型：
--
作者：
Summy-Long,JY;Denlinger,C;Palm,D;Hartman,RD;Rosella-Dampman,LM
内源性阿片肽在脱水、出血和分娩过程中抑制催产素的分泌，并减弱尾部电击引起的加压素的释放。不同的代理人被用来刺激下丘脑-神经垂体系统调查的假设，如果催产素（或加压素）的释放被阿片肽抑制，无论刺激，阿片类药物的作用的网站可能是在最后的共同途径（即大细胞神经元）或垂体细胞在神经叶。因此，我们使用雄性Sprague-Dawley大鼠，研究阿片受体拮抗剂纳洛酮（5 mg/kg s.c.）对各种药理学刺激升高的催产素和加压素血浆浓度的影响，包括组胺（10 mg/kg i. p.），尼古丁（0.15或1.5 mg/kg i. p.），异丙肾上腺素（30或120 ug/kg i.m.）脑脊液（CSF; 10 µl含1 MNaCl的人工CSF i.v.t.）中[NaCl]增加。对照动物接受生理盐水（0.85%）或人工CSF（含0.16 MNaCl）。在刺激或媒介物后60秒（t1 [NaCl 2在CSF中]）或10分钟将动物断头。从血浆中提取加压素和催产素，并通过RIA进行定量。组胺、异丙肾上腺素（30和120 αg/ kg）、CSF中的↑[NaCl]和较高剂量（1.5 mg/kg）但不较低剂量（0.15 mg/kg）的尼古丁升高了血浆中催产素和加压素的浓度（p < 0.05）。在CSF中组胺、尼古丁（0.15和1.5 mg/kg）、异丙肾上腺素（30和120 µg/kg）和↑[NaCl]后，纳洛酮进一步增加血浆中催产素的浓度（p<0.05）。纳洛酮还增加接受CSF或盐水的对照组中的催产素浓度（p<0.05）。无论是在对照组还是在任何刺激后，加压素浓度都不受纳洛酮的影响。我们得出结论，内源性阿片肽抑制催产素在体内的释放的影响，最终共同的途径，即大细胞神经元或垂体细胞在神经叶。
Endogenous opioid peptides inhibit secretion of oxytocin during dehydration, hemorrhage and parturition and attenuate release of vasopressin by tail electroshock. Diverse agents were used to stimulate the hypothalamo-neurohypophysial system to investigate the hypothesis that if oxytocin (or vasopressin) release were inhibited by opioid peptides regardless of the stimulus, the site of opiate action may be in the final common pathway (i.e. the magnocellular neuron) or on pituicytes in the neural lobe. Using male Sprague-Dawley rats, we therefore investigated the effect of an opiate receptor antagonist, naloxone (5 mg/kg s.c), on the plasma concentrations of oxytocin and vasopressin elevated by various pharmacologic stimuli, including histamine (10 mg/kg i.p.), nicotine (0.15 or 1.5 mg/kg i.p.), isoproterenol (30 or 120 ug/kg i.m.) and increased [NaCl] in cerebrospinal fluid (CSF; 10 µl artificial CSF containing 1 MNaCl i.v.t.). Control animals received saline (0.85%) or artificial CSF (containing 0.16MNaCl). Animals were decapitated 60 s (†[NaCΓJ in CSF) or 10 min after the stimulus or vehicle. Vasopressin and oxytocin were extracted from plasma and quantified by RIA. The concentrations of oxytocin and vasopressin in plasma were elevated (p < 0.05) by histamine, isoproterenol (30 and 120 αg/ kg), ↑[NaCl] in CSF, and nicotine at the higher (1.5 mg/kg) but not lower (0.15 mg/kg) dose. Naloxone increased further (p<0.05) the concentration of oxytocin in plasma after histamine, nicotine (0.15 and 1.5 mg/kg), isoproterenol (30 and 120 µg/kg) and ↑[NaCl] in CSF. Naloxone also increased (p<0.05) oxytocin concentration in controls receiving CSF or saline. Vasopressin concentration was unaffected by naloxone in either controls or after any of the stimuli. We conclude that endogenous opioid peptides inhibit release of oxytocin in vivo by an effect on the final common pathway, i.e. the magnocellular neuron or on pituicytes in the neural lobe.