Inhibition of rat cardiac calcium pump activity by cationic amphiphilic drugs
Identifieur interne : 002E72 ( Main/Exploration ); précédent : 002E71; suivant : 002E73Inhibition of rat cardiac calcium pump activity by cationic amphiphilic drugs
Auteurs : Prasada Rao S. Kodavanti [États-Unis] ; Srinivas N. Pentyala [États-Unis] ; Prabhakara R. Yallapragada [États-Unis] ; Joseph A. Cameron [États-Unis] ; Durisala Desaiah [États-Unis]Source :
- Drug Development Research [ 0272-4391 ] ; 1992.
English descriptors
- Teeft :
- Active calcium transport, Amphiphilic, Arrhythmia, Calcium, Calcium transport, Calcium transport phenomenon, Calcium uptake, Cardiac, Cardiac calcium, Cardiac sarcoplasmic reticulum, Cationic, Cationic amphiphilic drugs, Cell biochem, Cell cardiol, Chlorimipramine, Chlorinated analog, Chlorinated analogs, Chloroquine, Chlorphentermine, Chlorpromazine, Control rats, Defective calcium, Dependent protein kinase, Desaiah, Different concentrations, Dose level, Drug effects, Equal volumes, Fine olivarius, Folinphenol reagent, Higher concentrations, Homogenizing medium, Hypersensitivity myocarditis, Imipramine, Kodavanti, Male rats, Mehendale, Methods section, Myocardial toxicity, Observable effects, Oral gavage, Phosphorylation, Present investigation, Present results, Protein phosphorylation, Reactive metabolite, Reticulum, Sarcoplasmic, Sarcoplasmic reticulum, Sodium azide, Tada, Therapeutic category, Therapeutic dose, Toxicity, Vesicular fragments, Vivo effects, Vivo studies.
Abstract
Cationic amphiphilic drugs such as imipramine, chlorimipramine, chlorpromazine, chlorphentermine, and chloroquine have been shown to cause myocardial toxicity including arrhythmia, cardiomyopathy, and myocarditis. Since calcium transport by sarcoplasmic reticulum (SR) plays a critical role in contraction‐relaxation coupling of myocardium, the toxicity exhibited by these drugs could be due to their effects on this phenomenon. Hence, we have studied the effects in vitro and in vivo of imipramine, chlorimipramine, chlorpromazine, chloroquine, and chlorphentermine on cardiac SR 45Ca‐uptake and Ca2+‐ATPase in male Fisher‐344 rats. For in vitro studies, cardiac SR was prepared from normal rat hearts. For in vivo studies, rats were treated with drugs by oral gavage (p.o) at a dose of 20 pair‐fed. All these drugs in vitro inhibited the cardiac SR 45Ca‐uptake to a varying extent. The order of potency is chlorimipramine > chlorpromazine > imipramine > chlorphentermine > chloroquine. The inhibitory pattern of these drugs on cardiac SR Ca2+‐ATPase also followed the same trend. The chlorinated analogs of these drugs are more potent in inhibiting 45Ca‐uptake as well as Ca2+‐ATPase as compared to their nonchlorinated con‐geners. In vivo, all the drugs except chloroquine inhibited the 45Ca‐uptake and Ca2+‐ATPase activity to a different extent. The inhibition of cardiac SR calcium pump activity was seen as early as 7 days of treatment with chlorimipramine whereas all the other drugs (imipramine, chlorpromazine, and chlorphentermine) inhibited this calcium pump only at 21 days of treatment. Although in vivo chloroquine‐induced inhibition of calcium pump activity did not reach significant level, it seems that there may be an effect at higher concentrations. In summary, the present results indicate that these cationic amphiphilic drugs might be exerting myocardial toxicity due to changes in cellular Ca2+ homeostasis because of their effects on cardiac SR calcium transport phenomenon. © 1992 Wiley‐Liss, Inc.
Url:
DOI: 10.1002/ddr.430260104
Affiliations:
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Kodavanti</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><placeName><region type="state">État du Mississippi</region></placeName><wicri:cityArea>Department of Biology, Jackson State University, Jackson</wicri:cityArea></affiliation><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><placeName><region type="state">Caroline du Nord</region></placeName><wicri:cityArea>Current Address: Neurotoxicology Division, MD # 74B, Health Effects Research Laboratory, U.S. Environment Protection Agency, Research Triangle Park</wicri:cityArea></affiliation></author><author><name sortKey="Pentyala, Srinivas N" sort="Pentyala, Srinivas N" uniqKey="Pentyala S" first="Srinivas N." last="Pentyala">Srinivas N. Pentyala</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><placeName><region type="state">État du Mississippi</region></placeName><wicri:cityArea>Department of Biology, Jackson State University, Jackson</wicri:cityArea></affiliation></author><author><name sortKey="Yallapragada, Prabhakara R" sort="Yallapragada, Prabhakara R" uniqKey="Yallapragada P" first="Prabhakara R." last="Yallapragada">Prabhakara R. Yallapragada</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><placeName><region type="state">État du Mississippi</region></placeName><wicri:cityArea>Department of Biology, Jackson State University, Jackson</wicri:cityArea></affiliation></author><author><name sortKey="Cameron, Joseph A" sort="Cameron, Joseph A" uniqKey="Cameron J" first="Joseph A." last="Cameron">Joseph A. Cameron</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><placeName><region type="state">État du Mississippi</region></placeName><wicri:cityArea>Department of Neurology, University of Mississippi Medical Center, Jackson</wicri:cityArea></affiliation></author><author><name sortKey="Desaiah, Durisala" sort="Desaiah, Durisala" uniqKey="Desaiah D" first="Durisala" last="Desaiah">Durisala Desaiah</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><placeName><region type="state">État du Mississippi</region></placeName><wicri:cityArea>Department of Biology, Jackson State University, Jackson</wicri:cityArea></affiliation><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><placeName><region type="state">État du Mississippi</region></placeName><wicri:cityArea>Correspondence address: Department of Neurology, University of Mississippi Medical Center, 2500 North State Street, Jackson</wicri:cityArea></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">Drug Development Research</title><title level="j" type="alt">DRUG DEVELOPMENT RESEARCH</title><idno type="ISSN">0272-4391</idno><idno type="eISSN">1098-2299</idno><imprint><biblScope unit="vol">26</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="49">49</biblScope><biblScope unit="page" to="59">59</biblScope><biblScope unit="page-count">11</biblScope><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="1992">1992</date></imprint><idno type="ISSN">0272-4391</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0272-4391</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Active calcium transport</term><term>Amphiphilic</term><term>Arrhythmia</term><term>Calcium</term><term>Calcium transport</term><term>Calcium transport phenomenon</term><term>Calcium uptake</term><term>Cardiac</term><term>Cardiac calcium</term><term>Cardiac sarcoplasmic reticulum</term><term>Cationic</term><term>Cationic amphiphilic drugs</term><term>Cell biochem</term><term>Cell cardiol</term><term>Chlorimipramine</term><term>Chlorinated analog</term><term>Chlorinated analogs</term><term>Chloroquine</term><term>Chlorphentermine</term><term>Chlorpromazine</term><term>Control rats</term><term>Defective calcium</term><term>Dependent protein kinase</term><term>Desaiah</term><term>Different concentrations</term><term>Dose level</term><term>Drug effects</term><term>Equal volumes</term><term>Fine olivarius</term><term>Folinphenol reagent</term><term>Higher concentrations</term><term>Homogenizing medium</term><term>Hypersensitivity myocarditis</term><term>Imipramine</term><term>Kodavanti</term><term>Male rats</term><term>Mehendale</term><term>Methods section</term><term>Myocardial toxicity</term><term>Observable effects</term><term>Oral gavage</term><term>Phosphorylation</term><term>Present investigation</term><term>Present results</term><term>Protein phosphorylation</term><term>Reactive metabolite</term><term>Reticulum</term><term>Sarcoplasmic</term><term>Sarcoplasmic reticulum</term><term>Sodium azide</term><term>Tada</term><term>Therapeutic category</term><term>Therapeutic dose</term><term>Toxicity</term><term>Vesicular fragments</term><term>Vivo effects</term><term>Vivo studies</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Cationic amphiphilic drugs such as imipramine, chlorimipramine, chlorpromazine, chlorphentermine, and chloroquine have been shown to cause myocardial toxicity including arrhythmia, cardiomyopathy, and myocarditis. Since calcium transport by sarcoplasmic reticulum (SR) plays a critical role in contraction‐relaxation coupling of myocardium, the toxicity exhibited by these drugs could be due to their effects on this phenomenon. Hence, we have studied the effects in vitro and in vivo of imipramine, chlorimipramine, chlorpromazine, chloroquine, and chlorphentermine on cardiac SR 45Ca‐uptake and Ca2+‐ATPase in male Fisher‐344 rats. For in vitro studies, cardiac SR was prepared from normal rat hearts. For in vivo studies, rats were treated with drugs by oral gavage (p.o) at a dose of 20 pair‐fed. All these drugs in vitro inhibited the cardiac SR 45Ca‐uptake to a varying extent. The order of potency is chlorimipramine > chlorpromazine > imipramine > chlorphentermine > chloroquine. The inhibitory pattern of these drugs on cardiac SR Ca2+‐ATPase also followed the same trend. The chlorinated analogs of these drugs are more potent in inhibiting 45Ca‐uptake as well as Ca2+‐ATPase as compared to their nonchlorinated con‐geners. In vivo, all the drugs except chloroquine inhibited the 45Ca‐uptake and Ca2+‐ATPase activity to a different extent. The inhibition of cardiac SR calcium pump activity was seen as early as 7 days of treatment with chlorimipramine whereas all the other drugs (imipramine, chlorpromazine, and chlorphentermine) inhibited this calcium pump only at 21 days of treatment. Although in vivo chloroquine‐induced inhibition of calcium pump activity did not reach significant level, it seems that there may be an effect at higher concentrations. In summary, the present results indicate that these cationic amphiphilic drugs might be exerting myocardial toxicity due to changes in cellular Ca2+ homeostasis because of their effects on cardiac SR calcium transport phenomenon. © 1992 Wiley‐Liss, Inc.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Caroline du Nord</li><li>État du Mississippi</li></region></list><tree><country name="États-Unis"><region name="État du Mississippi"><name sortKey="Kodavanti, Prasada Rao S" sort="Kodavanti, Prasada Rao S" uniqKey="Kodavanti P" first="Prasada Rao S." last="Kodavanti">Prasada Rao S. Kodavanti</name></region><name sortKey="Cameron, Joseph A" sort="Cameron, Joseph A" uniqKey="Cameron J" first="Joseph A." last="Cameron">Joseph A. Cameron</name><name sortKey="Desaiah, Durisala" sort="Desaiah, Durisala" uniqKey="Desaiah D" first="Durisala" last="Desaiah">Durisala Desaiah</name><name sortKey="Desaiah, Durisala" sort="Desaiah, Durisala" uniqKey="Desaiah D" first="Durisala" last="Desaiah">Durisala Desaiah</name><name sortKey="Kodavanti, Prasada Rao S" sort="Kodavanti, Prasada Rao S" uniqKey="Kodavanti P" first="Prasada Rao S." last="Kodavanti">Prasada Rao S. Kodavanti</name><name sortKey="Pentyala, Srinivas N" sort="Pentyala, Srinivas N" uniqKey="Pentyala S" first="Srinivas N." last="Pentyala">Srinivas N. Pentyala</name><name sortKey="Yallapragada, Prabhakara R" sort="Yallapragada, Prabhakara R" uniqKey="Yallapragada P" first="Prabhakara R." last="Yallapragada">Prabhakara R. Yallapragada</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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