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血管紧张素 II 对心血管系统中胰岛素样生长因子 I 表达的调节作用。

Angiotensin II Modulation of Insulin-like Growth Factor I Expression in the Cardiovascular System.

机构信息

Patrick Delafontaine, Marijke Brink, and Jie Du are at the Department of Medicine, Division of Cardiology, Emory University School of Medicine, 1639 Pierce Dr., 308 WMB,Atlanta, GA 30322USA.

出版信息

Trends Cardiovasc Med. 1996 Aug;6(6):187-93. doi: 10.1016/S1050-1738(96)00058-8.

Abstract

The renin-angiotensin system is important in the pathophysiology of hypertension, cardiac hypertrophy, heart failure, and vascular remodeling. Angiotensin II is a growth factor for vascular smooth muscle cells and for cardiac myocytes and non-myocytes. Recently, angiotensin II has been shown to interact at multiple levels with the insulin-like growth factor I (IGF-I) system. IGF-I is a major regulator of developmental growth, and of cellular metabolism and differentiation, acting by endocrine and autocrine/paracrine pathways. Angiotensin II activates IGF-I receptor signaling through multiple mechanisms, and this activation is required for the growth-promoting effects of angiotensin II on vascular smooth muscle. Angiotensin II also stimulates cardiac IGF-I gene expression. Contrary to its effects on vascular and cardiac IGF-I expression, angiotensin II depresses circulating IGF-I through a pressor-independent anorexigenic effect. The anorexigenic effect of angiotensin II, and an additional metabolic effect, produce marked weight loss in the angiotensin II-infused animal. The alterations in local and circulating IGF-I expression produced by angiotensin II are potentially of importance in understanding the pathophysiology of conditions in which the renin-angiotensin system is activated. (Trends Cardiovascular Med 1996;6:187-193).

摘要

肾素-血管紧张素系统在高血压、心肌肥厚、心力衰竭和血管重塑的病理生理学中起着重要作用。血管紧张素 II 是血管平滑肌细胞和心肌细胞及非心肌细胞的生长因子。最近,血管紧张素 II 已被证明在多个水平与胰岛素样生长因子 I(IGF-I)系统相互作用。IGF-I 是发育生长、细胞代谢和分化的主要调节剂,通过内分泌和自分泌/旁分泌途径发挥作用。血管紧张素 II 通过多种机制激活 IGF-I 受体信号转导,这种激活对于血管紧张素 II 对血管平滑肌的促生长作用是必需的。血管紧张素 II 还刺激心肌 IGF-I 基因表达。与对血管和心脏 IGF-I 表达的影响相反,血管紧张素 II 通过非加压性厌食作用抑制循环 IGF-I。血管紧张素 II 的厌食作用和另外的代谢作用导致输注血管紧张素 II 的动物体重明显减轻。血管紧张素 II 引起的局部和循环 IGF-I 表达的改变,对于理解肾素-血管紧张素系统激活的情况下的病理生理学可能具有重要意义。(心血管趋势杂志 1996 年;6:187-193)。

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