内皮素和血管紧张素Ⅱ对大鼠血管平滑肌细胞分裂的促进作用  

Potentiation of Proliferation of Vascular Smooth Muscle Cells Induced by Endothelin and Angiotensin n in Spontaneously

作　　者：孙双丹 许慧[1] 吴建明[1] 廖永伯 汤健[1] 唐朝枢[1] 

机构地区：[1]北京医科大学心肺内分泌研究室,北京100083

出　　处：《基础医学与临床》1993年第1期55-58,共4页Basic and Clinical Medicine

摘　　要：血管平滑肌细胞(SMC)的增生、肥厚是高血压的一个重要致病因素,但其机制尚不清楚。本工作选用自发性高血压大鼠(SHR)和其对照大鼠(WKY)培养的SMC,以细胞计数和[~3H]-Thymidine参入为指标,观察到内皮素(ET)和血管紧张素Ⅱ(ANGⅡ)以剂量依赖方式刺激SMC的增殖和细胞内DNA合成,但其效应在SHR SMC更明显;心钠素(ANF)可显著抑制上述效应。SHR SMC对ET和ANGⅡ促分裂作用的反应性增强以及ANF对其抑制效应提示,ET和ANGⅡ的促血管壁增生作用在高血压的发生发展中起着重要作用,ANF可能具有机体内源性抗高血压因子的作用,抑制和缓解高血压的发生发展。In order to determine whether the morphological alteration observed in arterial media of spontaenously hypertensive rats (SHR) could be induced by an abnormal response of the smooth muscle cells to endogenous vasoactive agents, we studied the action of endothelin (ET) and angiolensin Ⅱ (ANG Ⅱ) on cultured aortic smooth muscle cells (SMC) from both SHR and Wistar-Kyolo rats (WKY) by means of cell counting and 3H-thymidine incorporation. Under our experimental conditions, ETand ANG Ⅱ exerts a mitogenic action on the cells, whereas its effect is more powerful in SHR than in WKY. This effect is inhibited by co-incubation with atrial natriure-tic factor (ANF) . The hyperresponsiveness in SHR to the mitogenic activ ty of ET and ANG Ⅱ , as well as the inhibition of ANF on this effect suggest that the excessive proliferation of SMC induced by ET and ANG Ⅱ may be an important role in the development of hypertension, anc ANF, like an endogenous antihyperlen-sive factor, inhibits or mitigates the hypertension formation.

关 键 词：高血压 内皮素 血管紧张素 

分 类 号：R544.1[医药卫生—心血管疾病]