摘要
测定６２例高血压病（ＥＨ）患者，２０例正常对照者（ＮＴ），２０例有和无高血压家族史的正常血压子女（ＦＨ＋１０例，ＦＨ－１０例）的血小板各组份的基础蛋白激酶Ｃ（ＰＫＣ）活性，并观察ＰＫＣ激动剂ｐｈｏｒｂｏｌ－１２－ｍｙｒｉｓｔａｔｅ－１３－ａｃｅｔｕｔｅ（ＰＭＡ）作用后的ＰＫＣ激发变化。结果显示，ＥＨ组血小板质膜基础ＰＫＣ活性及ＰＭＡ刺激后血小板胞液ＰＫＣ活性激发值均显著高于ＮＴ组，提示高血压时存在血小板ＰＫＣ活性增加现象，尤其是ＦＨ＋组对ＰＭＡ的敏感性异常增加可能与该类子女的遗传易感性增加有关。
Abstract Considerable evidence suggests that protein kinase C(PKC) activation participates in the regulation of vascular smooth muscle tone.We measured protein kinase C (PKC) activity in platelets in 62 essential hypertensive patietns(EH group), 20 normotensive subjects(NT group)and 20 normotensive offsprings with (FH￣+group, n=10) and without (FH￣- group , n=10) a family history of essential hypertension. The main findings were as followings. (1) PKC activities in the cytosol fraction of platelets were not different between EH and NT group (P>0.05). Cytosol fraction stimulated with PKC activator phorbol-12-myristate-13-acetate (PMA)leads marked elevation in EH. (2) PKC activities in the membrane fraction of platelets in EH were increased (497. 95±103.90 pmol/min/mg protein) compared with NT (416. 87±73. 50 pmol/min/mg protein , P<0. 01),and the activity was the greatest in stage Ⅲ hypertension (553. 38±110. 49 pmol/min/mg protein).(3) The only difference between FH￣- and FH￣+ groups was that of the cytosol fraction stimulated with PMA,FH￣+ group was increased compared with that in FH￣-group (486. 86±74.41,404.35±83.10 pmol/min/mg protein,P<0.01) . These results suggest that PKC activation may be involved in the regulation of vascular smooth musle tone; the increased sensitivity to PMAmediated activity in FH￣+ group may be responsible for a genetic predisposition to hypertension.
出处
《中华心血管病杂志》
CAS
CSCD
北大核心
1995年第5期339-341,共3页
Chinese Journal of Cardiology
基金
上海市高教局基金
