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, N Balta, V Filcescu, I F Dumitriu, G Stoian, 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.