林乐健, 唐发宽. 血管紧张素Ⅱ1型受体拮抗剂氯沙坦降低自发性高血压大鼠血管的肌源性紧张度的作用[J]. 心脏杂志, 2010, 22(6): 838-841.
    引用本文: 林乐健, 唐发宽. 血管紧张素Ⅱ1型受体拮抗剂氯沙坦降低自发性高血压大鼠血管的肌源性紧张度的作用[J]. 心脏杂志, 2010, 22(6): 838-841.
    Angiotensin II type-1 receptor blockade decreases arterial myogenic tone in spontaneously hypertensive rats[J]. Chinese Heart Journal, 2010, 22(6): 838-841.
    Citation: Angiotensin II type-1 receptor blockade decreases arterial myogenic tone in spontaneously hypertensive rats[J]. Chinese Heart Journal, 2010, 22(6): 838-841.

    血管紧张素Ⅱ1型受体拮抗剂氯沙坦降低自发性高血压大鼠血管的肌源性紧张度的作用

    Angiotensin II type-1 receptor blockade decreases arterial myogenic tone in spontaneously hypertensive rats

    • 摘要: 目的: 观察血管紧张素Ⅱ(AngⅡ)1型受体阻断剂氯沙坦对自发性高血压(SH)大鼠大脑中动脉血管肌源性紧张度的影响。方法: 16只SH Wistar大鼠随机分为SH组(n=8)和30 mg/(kg·d)氯沙坦干预(LI)组(n=8),另以8只正常WKY大鼠作为对照组,10周后,采用压力型小动脉测量仪在含2.5 mmol/L Ca2+或无Ca2+的生理盐溶液中,测量不同管腔压力下血管的主动态管径(active diameter,Da)和被动态管径(passive diameter,Dp)。肌源性紧张度以(Dp-Da)/Dp×100%表示。结果: SH大鼠大脑中动脉血管的肌源性紧张度同对照组相比升高67.9%,每天通过灌胃给予30 mg/(kg·d)的氯沙坦能够使SH大鼠大脑中动脉血管的肌源性紧张度降低24.9%。结论: SH大鼠大脑中动脉血管的肌源性紧张度同对照组相比显著增加,每天给予30 mg/(kg·d)的氯沙坦能够防止这种改变,说明肾素-血管紧张素-醛固酮系统参加了SH大鼠血管功能的重建过程,AngⅡ1型受体是其中重要的信号转导通路。

       

      Abstract: AIM:To investigate the effects of angiotensin II type-1 receptor blocker on arterial myogenic tone of spontaneously hypertensive rats (SHR). METHODS: Sixteen SHR rats (8 weeks of age) were randomly divided into losartan 30 mg/(kg·day) group (SHR+L) and normal SHR group (SHR), and eight sex- and age-matched Wistar rats were assigned to control group (CON). Rats assigned to CON and SHR groups received vehicle (distilled water) by gavage, and distilled water containing losartan at 30 mg/(kg·day) was administered to rats in SHR+L groups. After 10 weeks, segments of middle cerebral artery were isolated and then cannulated to two pipettes. Vascular diameters in response to the increased intraluminal pressure (from 0 mmHg to 125 mmHg in 25-mmHg increments) of isolated middle cerebral arteries under no-flow conditions were recorded by a Pressure Myograph System both in physiological salt solution (PSS) (active diameter, Da) and calcium-free PSS (passive diameter, Dp). Myogenic tone was calculated by (Dp-Da)/Dp×100%. RESULTS: Myogenic tone responsiveness of middle cerebral artery in SHR group increased significantly compared with that in CON group, with 30 mg/(kg·day) losartan treatment in SHR+L group. This enhancement may be partially prevented. CONCLUSION: RAS (spell out) participates in arterial function remodeling in SHRs. Chronic AT1 receptor antagonist therapy with losartan markedly reduces the changes of function in SHRs.

       

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