The development of new method of IP4 detection and the study of its intracellular distribution.
The development of new method of IP4 detection and the study of its intracellular distribution.
批准号:
01870041
负责人:
KAWAGUCHI Hideaki
金额:
$11.71万
依托单位:
依托单位国家:
日本
项目类别:
Grant-in-Aid for Developmental Scientific Research
财政年份:
1989
资助国家:
日本
项目状态:
已结题
起止时间:
1989 至 1990
中文摘要
目的:细胞内游离钙离子在细胞增殖过程中起重要作用。三磷酸肌醇(IP 3)是肌浆网(SR)释放胞内Ca^2+进入胞浆的第二信使。本研究通过测定IP 3刺激的肥厚大鼠心肌SR Ca^2+释放,探讨心肌肥厚与Ca^2+释放的关系。设计与方法:实验采用10-30周龄雄性自发性高血压大鼠(SHR)和同龄正常血压Wistar-kyoto大鼠(WKY)。将大鼠心脏匀浆并在105,000 xg下离心90 min。将所得沉淀用作SR组分。从用α 1-阻断剂盐酸布纳齐辛(10 mg/Kg体重/天)或β-阻断剂阿替洛尔(20 mg/Kg体重/天)处理的SHR中也获得SR组分。结果:在1 M的IP 3下检测到由IP 3刺激的Ca^<2+>释放。释放呈剂量依赖性增加5 M或IP 3。10-30周龄SHR的释放量高于同龄WKY,SHR经α或β受体阻滞后左室重量明显减轻。IP 3刺激的Ca^<2+>释放在降压药治疗的SHR中也被显著抑制。结论:本实验结果提示,IP 3和Ca^<2+>在SHR心肌肥厚中起重要作用。
英文摘要
Objective : Free cytosolic calcium plays an important role in the development of cell proliferation. Inositol 1,4,5-trisphosphate (IP3) is a second messenger releasing intracellular Ca^<2+> into the cytosol from sarcoplasmic reticulum (SR). We determined Ca^<2+> release from SR stimulated by IP3 in hypertrophied rat heart to investigate the relationship between cardiac hypertrophy and Ca^<2+>Design and Methods : Experiments were carried out on 10-30-week-old male spontaneously hypertensive rat (SHR) and age-matched normotensive Wistar-kyoto rat (WKY). Rat heart was homogenized and centrifuged at 105,000xg for 90 min. The resultant pellets were used as SR fraction. SR fractions were also obtained from SHR treated with alpha 1-blockade, bunazisin-HC1 (10 mg/Kg body weight/day) or beta-blockade, atenolol (20 mg/Kg body weight/day)Results : Ca^<2+> release stimulated by IP3 was detected at 1 M of IP3. The release was dose dependently increased by 5 M or IP3. The release was higher in 10-30 weeks old SHR compared with agematched WKY.Left ventricular weight was markedly decreased in SHR treated with alpha- or beta-blockade. Ca^<2+> release stimulated with IP3 was also suppressed in these SHR treated with antihypertensive drugs, significantly. Now we have been trying to purify IP4 binding protein.Conclusion : These results may suggest that IP3 and Ca^<2+> have an important role in cardiac hypertrophy in SHR.
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H Kawaguchi: "Streptokinase stimulated phospholipase C activity in pulmonary artery endothelial cell" Biochim Biophys Acta. 1055. 223-229 (1990)
H Kawaguchi:“链激酶刺激肺动脉内皮细胞中的磷脂酶 C 活性”Biochim Biophys Acta。
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H Takano: "Effect of calcium activated neutral protease inhibitor on platelet aggregation activated by PAF" Biochem Med Med Biol. 45. 41-47 (1990)
H Takano:“钙激活中性蛋白酶抑制剂对 PAF 激活的血小板聚集的影响”Biochem Med Med Biol。
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H.Kawaguchi: "Streptokinase stimulated phosholipase Cactivity in pulmonary artery ondothelial all" Biochim Biophys Acta. 1055. 223-229 (1990)
H.Kawaguchi:“链激酶刺激肺动脉上皮细胞中的磷脂酶活性”Biochim Biophys Acta。
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Kinito Takahashi: "The hypertensive response to vasopressor agents stimutes the release of thromboxne A_2 in hypercholesterolaemic rabbits" Cardiovascular Research. 23. 788-796 (1989)
Kinito Takahashi:“血管加压药的高血压反应会刺激高胆固醇血症兔子释放血栓素 A_2”心血管研究。
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H.Kawaguchi: "Effect of endothelin on angiotensin converting enzyme activity in cultured pulmonary artery endothetial cells" Journal of Hypertension. 9. 171-174 (1991)
H.Kawaguchi:“内皮素对培养的肺动脉内皮细胞中血管紧张素转换酶活性的影响”高血压杂志。
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共 17 条
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