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室旁核在肾传入神经升压反应中的作用。

Contribution of paraventricular nucleus to afferent renal nerve pressor response.

作者信息

Caverson M M, Ciriello J

机构信息

Department of Physiology, University of Western Ontario, London, Canada.

出版信息

Am J Physiol. 1988 Mar;254(3 Pt 2):R531-43. doi: 10.1152/ajpregu.1988.254.3.R531.

Abstract

Experiments were done in alpha-chloralose-anesthetized, paralyzed, and artificially ventilated cats to determine the effect of afferent renal nerve (ARN) stimulation on the firing frequency of neurons in the paraventricular nucleus of the hypothalamus (PVH), whose axons project directly to the neurohypophysis (NH), and the contribution of these neurons to the pressor response elicited by ARN stimulation. In the first series of experiments, 474 single units were extracellularly recorded in the PVH region. Of these units 86 were antidromically excited by stimulation of the NH. Seventeen of the antidromic units (20%) responded orthodromically to ARN stimulation; 10 responded to ARN stimulation only, and 7 units responded to both ARN and buffer nerve stimulation. All PVH-NH-projecting neurons that responded to ARN stimulation were excited. In the second series the contribution of PVH neurons to the pressor response elicited by ARN stimulation was investigated in animals with the aortic depressor, carotid sinus, vagus, and cervical sympathetic nerves cut bilaterally. The ARN pressor response has previously been shown to be due to the activation of the sympathetic nervous system and to the release of arginine vasopressin (AVP). The primary and secondary (AVP component) components of the pressor response were attenuated by 51 and 69%, respectively, by bilateral injections of procaine hydrochloride into PVH or bilateral electrolytic lesions of PVH. Control injections of saline into PVH or electrolytic lesions of hypothalamic regions anterior, dorsal, or ventral to PVH did not alter the ARN pressor response. These experiments demonstrate that sensory information originating in renal receptors excites magnocellular neurosecretory neurons in PVH and suggest that this renal-paraventricular reflex loop may contribute to the elevated arterial pressure and AVP release during conditions when ARN are activated.

摘要

实验在使用α-氯醛糖麻醉、麻痹并进行人工通气的猫身上进行,以确定肾传入神经(ARN)刺激对下丘脑室旁核(PVH)中神经元放电频率的影响,PVH神经元的轴突直接投射到神经垂体(NH),并确定这些神经元对ARN刺激引发的升压反应的作用。在第一组实验中,在PVH区域细胞外记录了474个单个神经元。其中86个神经元通过刺激NH产生逆向兴奋。17个逆向兴奋的神经元(20%)对ARN刺激产生顺向反应;10个仅对ARN刺激有反应,7个神经元对ARN和缓冲神经刺激均有反应。所有对ARN刺激有反应的PVH-NH投射神经元均被兴奋。在第二组实验中,在双侧切断主动脉降压神经、颈动脉窦神经、迷走神经和颈交感神经的动物身上,研究了PVH神经元对ARN刺激引发的升压反应的作用。先前已证明,ARN升压反应是由于交感神经系统的激活以及精氨酸加压素(AVP)的释放。通过向PVH双侧注射盐酸普鲁卡因或对PVH进行双侧电解损伤,升压反应的初级成分和次级成分(AVP成分)分别减弱了51%和69%。向PVH注射生理盐水或对PVH前方、背侧或腹侧的下丘脑区域进行电解损伤作为对照,并未改变ARN升压反应。这些实验表明,源自肾感受器的感觉信息可兴奋PVH中的大细胞神经分泌神经元,并提示当ARN被激活时,这种肾-室旁核反射回路可能导致动脉血压升高和AVP释放。

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