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心房利钠肽对基础状态下及脱水诱导的血管加压素分泌的抑制作用并非由下丘脑结节垂体或结节漏斗多巴胺能神经元介导。

Atrial natriuretic peptide-induced suppression of basal and dehydration-induced vasopressin secretion is not mediated by hypothalamic tuberohypophysial or tuberoinfundibular dopaminergic neurons.

作者信息

Manzanares J, Lookingland K J, Moore K E

机构信息

Department of Pharmacology and Toxicology, Michigan State University, East Lansing 48824.

出版信息

Brain Res. 1990 Sep 10;527(1):103-8. doi: 10.1016/0006-8993(90)91066-p.

Abstract

The purpose of this study was to examine the effects of atrial natriuretic peptide (ANP) on the secretion of vasopressin and the activities of hypothalamic tuberohypophysial and tuberoinfundibular dopaminergic neurons in normal and dehydrated male rats. Neuronal activity was estimated by measuring the concentrations of 3,4-dihydroxyphenylacetic acid (DOPAC) and dopamine (DA) in brain and posterior pituitary regions containing terminals of tuberohypophysial (neural lobe; intermediate lobe) and tuberoinfundibular (median eminence) DA neurons. Intracerebroventricular (icv) administration of 20 micrograms ANP decreased basal arginine vasopressin concentrations in the plasma, but had no effect on the concentrations of DOPAC or DA in any region examined. Water deprivation caused a time-dependent increase in plasma arginine vasopressin concentrations, with maximal levels measured 2 days after removal of water bottles. Water deprivation had no effect on DOPAC concentrations in the neural lobe, intermediate lobe or median eminence, but increased DA concentrations in the neural lobe. ANP (20 micrograms/rat; icv) decreased arginine vasopressin concentrations in the plasma of water-deprived rats without altering DOPAC or DA concentrations in the neural lobe, intermediate lobe or median eminence. These results indicate that ANP-induced suppression of basal and dehydration-induced vasopressin secretion is not mediated by tuberohypophysial or tuberoinfundibular DA neurons.

摘要

本研究的目的是检测心房利钠肽(ANP)对正常和脱水雄性大鼠血管升压素分泌以及下丘脑结节垂体和结节漏斗多巴胺能神经元活性的影响。通过测量包含结节垂体(神经叶;中间叶)和结节漏斗(正中隆起)多巴胺能神经元终末的脑区和垂体后叶区域中3,4 - 二羟基苯乙酸(DOPAC)和多巴胺(DA)的浓度来评估神经元活性。脑室内(icv)注射20微克ANP可降低血浆中基础精氨酸血管升压素的浓度,但对所检测的任何区域中DOPAC或DA的浓度均无影响。禁水导致血浆精氨酸血管升压素浓度随时间增加,在移除水瓶后2天测得最高水平。禁水对神经叶、中间叶或正中隆起中DOPAC的浓度无影响,但增加了神经叶中DA的浓度。ANP(20微克/大鼠;icv)可降低禁水大鼠血浆中精氨酸血管升压素的浓度,而不改变神经叶、中间叶或正中隆起中DOPAC或DA的浓度。这些结果表明,ANP诱导的基础和脱水诱导的血管升压素分泌抑制并非由结节垂体或结节漏斗多巴胺能神经元介导。

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