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["激活“沉默”的血管收缩性5-羟色胺1A受体作为血管紧张素II和血清素对血管张力协同作用的一种可能机制"]

[Activation of "silent" vasoconstrictive 5-HT1A receptors as a possible mechanism of synergism in angiotensin II and serotonin effect on vascular tone].

作者信息

Kozhevnikova L M, Sukhanova I F, Avdonin P V

出版信息

Izv Akad Nauk Ser Biol. 2011 Jan-Feb(1):68-76.

PMID:21446059
Abstract

It has been shown that the agonist of 5HT1A-receptors 8-OH-DPAT induces contraction of aortic rings in the presence of angiotensin II. This effect is not associated with activation of alpha1-adrenoceptors by 8-OH-DPAT as it is reproduced in the presence of prazosin which completely suppresses the nonspecific vasoconstrictive effect of 8-OH-DPAT via alpha1-adrenoceptors on the aorta incubated without angiotensin II. Synergism in the action of angiotensin II and 8-OH-DPAT is completely preserved after partial desensitization of the receptors of angiotensin II. It has been found that 8-OH-DPAT increases the free cytoplasmic calcium concentration in cultured smooth muscle cells from the rat aorta. The data obtained support the hypothesis about the existence of "silent" vasoconstrictive 5HT1A-receptors. It has been suggested that activation of these receptors underlies synergism in vasoconstrictive action of serotonin and angiotensin II.

摘要

已表明,5-羟色胺1A受体激动剂8-羟基二苯丙氨酸(8-OH-DPAT)在血管紧张素II存在的情况下可诱导主动脉环收缩。这种效应与8-OH-DPAT对α1肾上腺素能受体的激活无关,因为在哌唑嗪存在的情况下也会出现这种效应,哌唑嗪可完全抑制8-OH-DPAT通过α1肾上腺素能受体对无血管紧张素II孵育的主动脉产生的非特异性血管收缩作用。在血管紧张素II受体部分脱敏后,血管紧张素II和8-OH-DPAT作用中的协同作用仍完全保留。已发现8-OH-DPAT可增加大鼠主动脉培养的平滑肌细胞中游离细胞质钙浓度。所获得的数据支持关于存在“沉默”血管收缩性5-羟色胺1A受体的假说。有人提出,这些受体的激活是血清素和血管紧张素II血管收缩作用协同作用的基础。

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