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脊髓上血管加压素和谷氨酸能神经元在大鼠轻度出血后肾交感神经活动增加中的作用。

The role of supraspinal vasopressin and glutamate neurones in an increase in renal sympathetic activity in response to mild haemorrhage in the rat.

作者信息

Yang Zhou, Coote J H

机构信息

Medical College, University of Nankai, Tianjin, PR China.

出版信息

Exp Physiol. 2006 Jul;91(4):791-7. doi: 10.1113/expphysiol.2006.034082. Epub 2006 May 12.

Abstract

This study investigated the importance of supraspinal vasopressin and glutamate neurones in regulating renal sympathetic activity as part of the response to an acute reduction in blood volume. Wistar rats anaesthetized with chloralose and urethane were instrumented to record arterial blood pressure, heart rate and left renal sympathetic nerve activity. Pharmacological agonists and antagonists to glutamate and vasopressin were applied to the renal outflow of the spinal cord via an intrathecal catheter inserted at the foramen magnum and with the tip at the level of T10. Both glutamate and vasopressin increased renal sympathetic activity, and these actions were shown to be selectively blocked by their respective antagonists. Removing 1 ml of venous blood from a femoral venous catheter elicited an increase of 26 +/- 2% in renal sympathetic activity. This response to mild haemorrhage was halved to 13 +/- 4% by prior intrathecal application of a selective V1a antagonist. Similarly, prior intrathecal application of kynurenic acid reduced the response to the mild haemorrhage from 28 +/- 2 to 12.6 +/- 2.8%. Intrathecal application of both antagonists together reduced the haemorrhage response even further to 8 +/- 3%. All the changes were statistically significant at P < 0.01. It is concluded that a small reduction in blood volume induces an increase in renal sympathetic activity dependent on vasopressin and glutamate release from terminals of supraspinal neurones. It is suggested that the vasopressin neurones most probably originate from the paraventricular nucleus of the hypothalamus.

摘要

本研究探讨了脊髓上血管加压素和谷氨酸能神经元在调节肾交感神经活动中的重要性,这是对血容量急性减少反应的一部分。用氯醛糖和乌拉坦麻醉的Wistar大鼠被植入仪器以记录动脉血压、心率和左肾交感神经活动。通过插入枕骨大孔且尖端位于T10水平的鞘内导管,将谷氨酸和血管加压素的药理激动剂和拮抗剂应用于脊髓的肾传出神经。谷氨酸和血管加压素均增加肾交感神经活动,并且这些作用被证明可被其各自的拮抗剂选择性阻断。从股静脉导管抽取1 ml静脉血可使肾交感神经活动增加26±2%。预先鞘内应用选择性V1a拮抗剂可使这种对轻度出血的反应减半至13±4%。同样,预先鞘内应用犬尿氨酸可使对轻度出血的反应从28±2%降低至12.6±2.8%。同时鞘内应用两种拮抗剂可使出血反应进一步降低至8±3%。所有变化在P<0.01时具有统计学意义。得出的结论是,血容量的小幅减少会导致肾交感神经活动增加,这依赖于脊髓上神经元终末释放的血管加压素和谷氨酸。有人提出血管加压素神经元很可能起源于下丘脑室旁核。

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