Activity of Na+/K+-ATPase and of Ca++-ATPase under the action of adenosine triphosphate in experimental myocardial hypertrophy.

C Moisin, N Balta, V Filcescu, I F Dumitriu, G Stoian, G Petec
{"title":"Activity of Na+/K+-ATPase and of Ca++-ATPase under the action of adenosine triphosphate in experimental myocardial hypertrophy.","authors":"C Moisin,&nbsp;N Balta,&nbsp;V Filcescu,&nbsp;I F Dumitriu,&nbsp;G Stoian,&nbsp;G Petec","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>This paper presents the results of our research on the mechanisms involved in the modifications occurring in the activity of ionic pumps (Na+/K+-ATPase and Ca++-ATPase) at the level of the sarcolemma, the sarcoplasmic reticulum and mitochondrial membrane of the myocardial cell in experimental myocardial hypertrophy induced by isoproterenol. We also studied the effects of concomitant administration of adenosine triphosphate. Thus, we found the activity of the sarcolemmal Ca++-ATPase intensely increased under the action of isoproterenol, while Ca++-ATPase activity in the sarcoplasmic reticulum decreased significantly. At the same time, the Na+/K+-ATPase activity decreased both in the sarcolemma and in the sarcoplasmic reticulum. Administration of adenosine triphosphate induces opposite effects, of lower intensity, upon the activity of the two ATPase, that tend to offset the the effects of isoproterenol. This was found in the group of rats given concomitantly both isoproterenol and adenosine triphosphate. A better understanding of the processes involved in those modifications of membrane ATPase activity allows us to consider their different behaviour to isoproterenol and adenosine triphosphate as the expression of intrinsic mechanisms by means of which the myocardial cell intervenes in maintaining a physiological concentration of calcium ions (Ca++) that is necessary both in order to avoid a failure of the contractile apparatus and in order to preserve the mitochondria role of ATP supplier. Our results demonstrate the antiadrenergic action of adenosine triphosphate that attenuates isoproterenol effects on cardiac myocytes.</p>","PeriodicalId":79373,"journal":{"name":"Romanian journal of physiology : physiological sciences","volume":"35 3-4","pages":"303-11"},"PeriodicalIF":0.0000,"publicationDate":"1998-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Romanian journal of physiology : physiological sciences","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0

Abstract

This paper presents the results of our research on the mechanisms involved in the modifications occurring in the activity of ionic pumps (Na+/K+-ATPase and Ca++-ATPase) at the level of the sarcolemma, the sarcoplasmic reticulum and mitochondrial membrane of the myocardial cell in experimental myocardial hypertrophy induced by isoproterenol. We also studied the effects of concomitant administration of adenosine triphosphate. Thus, we found the activity of the sarcolemmal Ca++-ATPase intensely increased under the action of isoproterenol, while Ca++-ATPase activity in the sarcoplasmic reticulum decreased significantly. At the same time, the Na+/K+-ATPase activity decreased both in the sarcolemma and in the sarcoplasmic reticulum. Administration of adenosine triphosphate induces opposite effects, of lower intensity, upon the activity of the two ATPase, that tend to offset the the effects of isoproterenol. This was found in the group of rats given concomitantly both isoproterenol and adenosine triphosphate. A better understanding of the processes involved in those modifications of membrane ATPase activity allows us to consider their different behaviour to isoproterenol and adenosine triphosphate as the expression of intrinsic mechanisms by means of which the myocardial cell intervenes in maintaining a physiological concentration of calcium ions (Ca++) that is necessary both in order to avoid a failure of the contractile apparatus and in order to preserve the mitochondria role of ATP supplier. Our results demonstrate the antiadrenergic action of adenosine triphosphate that attenuates isoproterenol effects on cardiac myocytes.

三磷酸腺苷作用下心肌肥大Na+/K+- atp酶和Ca++- atp酶活性的变化。
本文介绍了异丙肾上腺素诱导实验性心肌肥大时心肌细胞肌膜、肌浆网和线粒体膜离子泵(Na+/K+- atp酶和Ca++- atp酶)活性变化的机制研究结果。我们还研究了同时服用三磷酸腺苷的效果。因此,我们发现在异丙肾上腺素作用下,肌层ca2 ++- atp酶活性强烈增加,而肌浆网ca2 ++- atp酶活性明显降低。同时,肌膜和肌浆网内Na+/K+- atp酶活性降低。三磷酸腺苷的施用对两种atp酶的活性产生相反的作用,其强度较低,往往会抵消异丙肾上腺素的作用。这是在同时给予异丙肾上腺素和三磷酸腺苷的大鼠组中发现的。更好地理解这些膜ATP酶活性修饰的过程,使我们能够考虑它们对异丙肾上腺素和三磷酸腺苷的不同行为,作为内在机制的表达,心肌细胞通过这种机制干预维持钙离子(ca++)的生理浓度,这是避免收缩装置失效和保持线粒体ATP供体作用所必需的。我们的研究结果表明,三磷酸腺苷的抗肾上腺素能作用可以减弱异丙肾上腺素对心肌细胞的作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
自引率
0.00%
发文量
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信