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血管α1D肾上腺素能受体表达和功能的增强可能介导血管紧张素II的升压作用。

Increased expression and function of vascular alpha1D-adrenoceptors may mediate the prohypertensive effects of angiotensin II.

作者信息

Villalobos-Molina Rafael, Ibarra Maximiliano

机构信息

Unidad de Biomedicina, Facultad de Estudios Superiores-Iztacala, Universidad Nacional Autónoma de Mexico, Tlalnepantla, México.

出版信息

Mol Interv. 2005 Dec;5(6):340-2. doi: 10.1124/mi.5.6.6.

Abstract

The peptide Angiotensin II (Ang II), part of the renin-angiotensin system (RAS), participates in the control of systemic arterial pressure. Ang II participates in increasing smooth muscle tone, and its positive effects on smooth muscle cell DNA synthesis are inhibited by treatment with prazosin, an alpha(1)-adrenoceptor agonist. Ang II also induces the expression of alpha(1)-adrenoceptor, especially the alpha(1D) subtype. Other findings suggest that the molecular signals activated by Ang II and by alpha(1D)-adrenoceptor might interweave, thus leading to the augmentation of smooth muscle tone and hypertension.

摘要

肽类血管紧张素II(Ang II)是肾素-血管紧张素系统(RAS)的一部分,参与全身动脉血压的调控。Ang II参与增加平滑肌张力,而其对平滑肌细胞DNA合成的积极作用会被α(1)-肾上腺素能受体激动剂哌唑嗪治疗所抑制。Ang II还可诱导α(1)-肾上腺素能受体的表达,尤其是α(1D)亚型。其他研究结果表明,由Ang II和α(1D)-肾上腺素能受体激活的分子信号可能相互交织,从而导致平滑肌张力增加和高血压。

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