Influence of atrial stretch receptors on hypothalamic neurosecretory neurones.

Influence of atrial stretch receptors on hypothalamic neurosecretory neurones.
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心房牵张受体对下丘脑神经分泌神经元的影响。

DOI:
10.1113/jphysiol.1978.sp012575
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发表时间:
1978
期刊:
The Journal of Physiology
影响因子:
--
通讯作者:
H. Yamashita
H. Yamashita
中科院分区:
--
文献类型:
--
作者:
K. Koizumi;H. Yamashita

文献摘要

被引文献

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1. 在麻醉的狗和猫中研究刺激心房受体对下丘脑神经分泌细胞的影响。通过拉伸左心房和右心房来激活心房受体,同时记录下丘脑视上核(s.o.n.)和室旁核(p.v.m.)中各个神经分泌神经元的动作电位。 2. 拉伸左心房可显着降低“逆向识别”s.o.n 的放电频率。和 p.v.n.狗和猫的神经元;狗中 98% 的神经元和猫中 70% 的神经元因此受到抑制。短暂反射性减速后心率加快。血压没有受到影响。心房舒张对 s.o.n 产生的抑制作用的大小和持续时间。和 p.v.n.神经元与心率中观察到的变化平行。 s.o.n 中大约三分之一的“未识别”细胞。和 p.v.n. (那些不能逆向激活的)被左心房拉伸所抑制。 3.双侧迷走神经切断术消除了对神经分泌神经元以及左心房拉伸产生的心率的影响,表明迷走神经携带传入冲动,导致观察到的变化。 4. 拉伸右心房不会导致 s.o.n 的发射频率发生变化。和 p.v.n.狗和猫的神经元,尽管心率因这种拉伸而大大增加。在同一只动物中连续测试左心房和右心房的刺激,以便比较不同的结果。 5. 研究了源自心房受体、压力感受器和化学感受器的反应的相互作用。在颈动脉闭塞或化学感受器刺激期间,神经分泌细胞的活性大大增强。然后进行左心房拉伸,引起 s.o.n 活动轻微或没有减少。和 p.v.n.神经元。这些结果被解释为压力或化学感受器对神经分泌神经元的影响可能比心房受体的影响更强。 6. 与在大鼠中进行的观察不同,在狗和猫中没有发现有节奏的爆发神经元(相位细胞)。然而,心房舒张有时会引起仅在舒张期间出现的节律性爆发模式。 7. 结论是,通过主要由迷走神经携带的传入冲动激活左心房受体,抑制 s.o.n 中的神经分泌神经元。和 p.v.n.讨论了这一发现与抗利尿激素 (ADH) 在维持血容量控制中的作用相关的意义。
1. The effects of stimulation of atrial receptors on hypothalamic neurosecretory cells were investigated in anaesthetized dogs and cats. Atrial receptors were activated by stretching the left and the right atria while action potentials of individual neurosecretory neurones in the supraoptic (s.o.n.) and paraventricular (p.v.m.) nuclei of the hypothalamus were recorded. 2. Stretching the left atrium markedly decreased firing frequencies of 'antidromically identified' s.o.n. and p.v.n. neurones in dogs and cats; 98% of neurones in dogs and 70% in cats were thus inhibited. Heart rate accelerated following a transient reflexly induced deceleration. The blood pressure was not affected. The magnitude and duration of inhibitory effects produced by atrial stretch on s.o.n. and p.v.n. neurones paralleled changes observed in heart rate. Approximately one third of 'unidentified' cells in s.o.n. and p.v.n. (those which could not be activated antidromically) were inhibited by left atrium stretch. 3. Bilateral vagotomy abolished the effects on neurosecretory neurones as well as on heart rate produced by left atrial stretch, indicating that the vagus nerves carry afferent impulses responsible for the observed changes. 4. Stretching the right atrium did not produce changes in firing frequencies of s.o.n. and p.v.n. neurones in dogs and cats, although cardiac rate was increased considerably by such stretch. Stimulation of the left and right atria was tested in the same animal in succession to permit comparison of the diverse results. 5. Interaction of responses originating from atrial receptors, baro‐ and chemoreceptors were studied. During carotid occlusion or stimulation of chemoreceptors activity of the neurosecretory cells was greatly augmented. Left atrial stretch when then applied evoked slight or no reduction in activity in s.o.n. and p.v.n. neurones. These results were interpreted to mean that the influence of baro‐ or chemoreceptors on neurosecretory neurones probably is stronger than that originating from atrial receptors. 6. Unlike the observations made in rats, no rhythmically bursting neurones (phasic cells) were found in dogs and cats. However, atrial stretch sometimes evoked a rhythmic bursting pattern which appeared only during stretch. 7. It is concluded that activation of left atrial receptors, through afferent impulses carried mainly by vagus nerves, inhibits neurosecretory neurones in s.o.n. and p.v.n. The implications of this finding in relation to the role of ADH in the maintenance of blood volume control were discussed.