HISTAMINERGIC NEUROMODULATION OF THE RELEASE OF VASOPRESSIN
HISTAMINERGIC NEUROMODULATION OF THE RELEASE OF VASOPRESSIN
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DOI：
10.1159/000124761
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发表时间：
1987-05-01
影响因子：
4.1
通讯作者：
WADA, H
中科院分区：
文献类型：
--
作者：
CACABELOS, R;YAMATODANI, A;WADA, H
为了阐明抗利尿激素系统中组胺能神经调节的本质，在不同的实验范式下进行了几项研究。l -组氨酸负荷（8 mmol/kg i.p.）诱导下丘脑前区（AHR）和后区（PHR）、中隆起区（ME）和腺垂体区（Ah）组胺（HA）显著升高，但对神经垂体区（Nh） HA浓度无明显影响。这些发现与AHR和ME中抗利尿激素（VP）水平的降低相关，并伴有PHR和Ah中神经肽的增加。腹腔注射HA （6 .mu）。mol/kg)，导致PHR、ME和Ah中VP水平显著（p < 0.005）升高。羟基磷灰石诱导前额叶皮层（PFC） VP从6.23 +-升高。2.02到43 .+-。4.05 .mu。U/mg，神经垂体VP降低60%。这些ha诱导的VP反应被mepyramine (3 .mu。Mol /kg)和法莫替丁(4 .mu。Mepyramine在Ah中抑制ha诱导的VP反应，在Nh中增强VP反应，而法莫替丁则相反。α -氟甲基组氨酸（FMH）是一种不可逆的组氨酸脱羧酶抑制剂，给药剂量为100 mg/kg/天（i.p）时，去肾上腺大鼠下丘脑HA水平在1小时后下降40-45%，3小时后下降50%，24小时后下降65-80%。在相同的条件下，但在FMH治疗一周后，VP对肾上腺切除术的反应明显受损。这些结果似乎表明，神经HA的生理水平对于神经内分泌系统的正常功能是不可或缺的。在这种情况下，初步的药理学证据表明，抗利尿激素系统的组胺能神经调节是通过Ah中的H1受体、ME和Nh中的H2受体以及PFC和下丘脑中的H1和H2受体介导的。
In an attempt to clarify the nature of histaminergic neuromodulation of the vasopressinergic system, several studies under different experimental paradigms were carried out. L-Histidine loads (8 mmol/kg i.p.) induced a marked increase in histamine (HA) in the anterior (AHR) and posterior (PHR) hypothalamic regions, the median eminence (ME) and adenohypophysis (Ah) with no apparent effect on the concentration of HA in the neurohypophysis (Nh), as measured by high-performance liquid chromatography. These findings correlated with decreases in vasopressin (VP) levels in the AHR and ME, accompanied by increases of the neuropeptide in the PHR and Ah. Intraperitoneal injections of HA (6 .mu.mol/kg), resulted in a significant (p < 0.005) rise in VP levels in the PHR, ME and Ah. HA induced an elevation of VP in the prefrontal cortex (PFC) from 6.23 .+-. 2.02 to 43 .+-. 4.05 .mu.U/mg, as well as a 60% reduction in neurohypophyseal VP. These HA-induced VP responses were abolished by both mepyramine (3 .mu.mol/kg) and famotidine (4 .mu.mol/kg) in the PHR and PFC. Mepyramine suppressed the HA-induced VP response in the Ah and enhanced it in the Nh, while famotidine did the opposite. When alpha-fluoromethylhistidine (FMH), an irreversible inhibitor of histidine decarboxylase, was administered at doses of 100 mg/kg/day (i.p.), hypothalamic HA levels fell by 40-45% after 1 h, by 50% after 3 h, and by 65-80% after 24 h in adrenalextomized rats. In the same conditions, but after a week of treatment with FMH, the VP response to adrenalectomy was clearly impaired. These results seem to demonstrate that the physiological levels of neuronal HA are indispensable for the normal functioning of the neuroendocrine system. In this context, preliminary pharmacological evidence showed that histaminergic neuromodulation of the vasopressinergic system is mediated through H1 receptors in the Ah, H2 receptors in the ME and Nh, and both H1 and H2 receptors in the PFC and hypothalamus.