摘要
目的:观察自发性高血压大鼠(SHR)血管平滑肌细胞Ca2+激活Cl-通道[ICl(Ca)]的活动。方法:测定离体肠系膜血管床灌注压和离体尾动脉肌条血管张力,以其对去甲肾上腺素(NE)收缩反应的变化作为舒缩活动的指标。结果:(1)SHR肠系膜动脉和尾动脉对NE收缩反应显著大于Wistar大鼠。(2)硝呋咪酸可显著抑制NE诱发的肠系膜动脉和尾动脉收缩反应,并具有浓度依赖性,SHR肠系膜动脉和尾动脉收缩活动受硝呋咪酸的抑制程度明显小于Wistar大鼠。(3)SHR肠系膜动脉对低氯缓冲液的反应显著大于Wistar大鼠。结论:SHR肠系膜动脉和尾动脉血管平滑肌的Ca2+激活Cl-通道的活动增强,并导致血管对NE的反应性增高。这可能是在高血压的发生过程中引起和维持较高血管张力和外周血流阻力的因素之一。
AIM： To study the chloride channel activity [ ICl（Ca）] in vascular smooth cells of the spontaneously hypertensive rats （SHR）. METHODS： The vascular beds of mesenteric arteries were isolated from the pentobarbital anesthetized rats and perfused with 37 ℃ PSS at a constant flow rate. The vasoconstriction response to norepinphrine （NE） was determined by changes in perfused pressure. The strips of the rat arteries were mounted in an organ chamber filled with 37 ℃ PSS and the vascular tension was measured. RESULTS： （ 1 ） The contractile responses of mesenteric arteries to NE in SHR were greater than that in Wistar rats. （2） The inhibitory magnitude of the contractile response by niflumic acid in SHR was significantly less than that in Wistar rats and showed dose- dependent manner. （＇3） Decreasing the extracellular C1- concentration increased the contractile response to NE significantly and the amplitude of enhanced contractile response in SHR was greater than that in Wistar rats. CONCLUSION： It can be concluded that NE- induced contraction is enhanced in SHR, which is partly due to an increase in Cl^- efllux through the Ca^2＋ - activated Cl^- channels. The chloride channel activity may increase in association with the elevation of vascular tone and blood pressure.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2005年第9期1705-1708,共4页
Chinese Journal of Pathophysiology
基金
山东省卫生系统九五攻关项目资助
关键词
氯化物通道
钙激活
去甲肾上腺素
尼氟灭酸
高血压
Chloride channels, calcium-activated
Norepinphrine
Niflumic acid
Hypertension
