低氧、血管紧张素Ⅱ对肺内小动脉平滑肌细胞膜Ca2+┐ATPase活力的影响  

EFFECTS OF HYPOXIA AND AngⅡON MEMBRANES ACTIVITY OF Ca 2+ ATPase IN CULTURED INTRA PULMONARY ARTERIOLAR SMOOTH MUSCLE CELLS

作　　者：胡德辉[1,2] 马传桃[1,2] 

机构地区：[1]湖南医科大学心血管生理研究室 [2]第一军医大学生理教研室

出　　处：《中国应用生理学杂志》1998年第4期316-319,共4页Chinese Journal of Applied Physiology

摘　　要：本课题观察了低氧及血管紧张素Ⅱ（ａｎｇｉｏｔｅｎｓｉｎⅡ，ＡｎｇⅡ）对分离培养家兔肺内小动脉平滑肌细胞（ＰＡＳＭ－Ｃｓ）膜Ｃａ２＋－ＡＴＰａｓｅ活力的影响，同时用钙通道阻断剂维拉帕米（ｖｅｒａｐａｍｉｌ，ＶＰ）进行干预，进一步了解细胞内钙与Ｃａ２＋－ＡＴＰａｓｅ活力的关系。结果表明：ＰＡＳＭＣｓ膜Ｃａ２＋－ＡＴＰａｓｅ活力对低氧具有短暂的耐受性，随低氧时间延长，Ｃａ２＋－ＡＴＰａｓｅ活力呈时间依赖性抑制；低氧、ＡＮＧⅡ均能抑制Ｃａ２＋－ＡＴＰａｓｅ活力（Ｐ＜０．０１）低氧＋ＡⅡ对Ｃａ２＋－ＡＴＰａｓｅ活力的抑制具叠加效应（Ｐ＜０．０５）；ＶＰ可逆转低氧、ＡｎｇⅡ、低氧＋ＡｎｇⅡ对Ｃａ２＋－ＡＴＰａｓｅ活力的抑制（Ｐ＜０．０１）。结果提示：低氧，ＡＮＧⅡ可通过抑制肺血管平滑肌细胞膜Ｃａ２＋－ＡＴＰａｓｅ活力而可能削弱肺血管平滑肌舒张功能也可能是低氧性肺动脉高压（ＨＰＨ）形成的原因之一。Cultured intra pulmonary arteriolar smooth muscle cells (PASMCs) were used to study the effects of hypoxia and angⅡ on actvity of Ca 2+ ATPase of PASMCs membrnes,along with being interfered with ve rapamil to reveale the relation between activity of Ca 2+ ATPase had adding intracellar calcium overload The result showed activity of Ca 2+ ATPase had transient resistance on hypoxia and it′s inbibition was depended on hypoxic duration, and it was also significantly inhibited by AngⅡ.Duplicated effect of inhibition was produced by hypoxia and AngⅡ.These effects were reversed by verapamil. Results suggested that inhibition of activity of Ca 2+ ATPase induced by hypoxia and AngⅡ and led to the disorder of dialated effect of pulmonary arteriolar smooth muscles and which was one of the pathogenesis of HPH.

关 键 词：低氧 AngⅡ Ca^2+ATPase 平滑肌细胞 肺内小动脉 

分 类 号：R329.26[医药卫生—人体解剖和组织胚胎学]