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儿茶酚胺能受体在前腹侧第三脑室区域介导前列腺素E2释放血管加压素及心血管作用中的作用可忽略不计。

Negligible role of catecholaminergic receptors in the anteroventral third ventricular region in mediating vasopressin-releasing and cardiovascular actions of prostaglandin E2.

作者信息

Yamaguchi K, Hama H, Watanabe K

机构信息

Department of Physiology, Niigata University School of Medicine, Japan.

出版信息

Exp Brain Res. 1999 Dec;129(4):532-40. doi: 10.1007/s002210050923.

Abstract

The aim of this study was to pursue the roles of the catecholamine receptors in the anteroventral third ventricular region (AV3V), a cerebral site engaged in various stress responses, in prostaglandin (PG) E2-evoked vasopressin (AVP) release and cardiovascular action. Experiments were conducted in conscious rats in which cerebral and vascular cannulae had been implanted chronically. Local infusion (0.5 microliter, 1 min) of dopamine (150 nmol), a D1-dopaminergic agonist SKF 38393 (17 nmol) and an alpha-adrenergic agonist phenylephrine (150 nmol), as well as PGE2 (7 nmol), into the AV3V enhanced plasma AVP 5 min later, without affecting plasma osmolality and electrolytes. In contrast to the increases in both arterial pressure and heart rate observed when PGE2 was applied, dopamine and SKF 38393 did not affect these variables, and phenylephrine elevated only arterial pressure. The AV3V infusion of a beta-agonist isoproterenol (100 nmol) did not change plasma AVP, although it decreased arterial pressure and increased heart rate. The increase in plasma AVP by dopamine was not blocked by the preinfusion of the D2-antagonist sulpiride (13 nmol) into the AV3V 10 min before, but was abolished by that of the D1-antagonist SCH-23390 (8 nmol). The effects of phenylephrine on both plasma AVP and the blood pressure were prevented by the preadministration of the alpha-antagonist phenoxybenzamine (13 nmol). However, the pretreatments with phenoxybenzamine, sulpiride or SCH 23390 did not inhibit the responses of AVP, arterial pressure and heart rate caused by PGE2. These antagonists were without significant effect on AVP and other variables when given alone. The infusion sites of PGE2 and the other drugs identified histologically included the AV3V structures such as the organum vasculosum laminae terminalis or its vicinity, median preoptic nucleus, medial preoptic nucleus and periventricular hypothalamic nucleus. Dopamine or phenylephrine administered into the cerebral ventricle at the same dose as used in the AV3V application did not exert a significant effect on plasma AVP, arterial pressure and heart rate. These results suggest that catecholamine receptors in the AV3V may not be involved in the AVP-secreting, tachycardiac and pressor responses evoked by topical action of PGE2 on this area, despite their ability to influence hormone release and cardiovascular function.

摘要

本研究旨在探讨儿茶酚胺受体在前腹侧第三脑室区域(AV3V)中的作用,该脑区参与多种应激反应,研究其在前列腺素(PG)E2诱发的血管加压素(AVP)释放及心血管作用中的角色。实验在长期植入脑和血管插管的清醒大鼠中进行。向AV3V局部注射(0.5微升,1分钟)多巴胺(150纳摩尔)、D1-多巴胺能激动剂SKF 38393(17纳摩尔)、α-肾上腺素能激动剂去氧肾上腺素(150纳摩尔)以及PGE2(7纳摩尔),5分钟后可使血浆AVP升高,且不影响血浆渗透压和电解质。与应用PGE2时观察到的动脉压和心率升高不同,多巴胺和SKF 38393对这些变量无影响,而去氧肾上腺素仅使动脉压升高。向AV3V注射β-激动剂异丙肾上腺素(100纳摩尔)虽可降低动脉压并增加心率,但并未改变血浆AVP。多巴胺引起的血浆AVP升高在10分钟前预先向AV3V注射D2拮抗剂舒必利(13纳摩尔)后未被阻断,但在预先注射D1拮抗剂SCH-23390(8纳摩尔)后被消除。预先给予α-拮抗剂酚苄明(13纳摩尔)可预防去氧肾上腺素对血浆AVP和血压的影响。然而,用酚苄明、舒必利或SCH 23390预处理并未抑制PGE2引起的AVP、动脉压和心率反应。这些拮抗剂单独给药时对AVP及其他变量无显著影响。组织学鉴定显示,PGE2和其他药物的注射部位包括AV3V结构,如终板血管器或其附近、视前正中核、视前内侧核和室旁下丘脑核。以与在AV3V应用相同的剂量向脑室注射多巴胺或去氧肾上腺素,对血浆AVP、动脉压和心率无显著影响。这些结果表明,尽管AV3V中的儿茶酚胺受体能够影响激素释放和心血管功能,但它们可能不参与PGE2局部作用于该区域所诱发的AVP分泌、心动过速和升压反应。

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