Phosphoinositide hydrolysis mediated by H1 receptors in autoimmune myocarditis mice

Stimulation of phosphoinositide hydrolysis in myocardium from autoimmune myocarditis mice by ThEA and histamine was assayed. Myocardium from autoimmune heart, but not the normal forms, specifically increased phosphoinositide turnover in the presence of histaminergic agonists. This increment was bloc...

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Main Authors: Nora Goren, Claudia Perez Leiros, Leonor Sterin-Borda, Enri S. Borda
Format: Article
Language:English
Published: Hindawi Limited 1993-01-01
Series:Mediators of Inflammation
Online Access:http://dx.doi.org/10.1155/S0962935193000444
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spelling doaj-1a8d55ef6ef344d9bd2442557c8a95aa2020-11-24T23:37:58ZengHindawi LimitedMediators of Inflammation0962-93511466-18611993-01-012431732210.1155/S0962935193000444Phosphoinositide hydrolysis mediated by H1 receptors in autoimmune myocarditis miceNora Goren0Claudia Perez Leiros1Leonor Sterin-Borda2Enri S. Borda3Centro de Estudios Farmacológicos y Botánicos (CEFYBO-CONICET), Serrano 665, Buenos Aires 1414, ArgentinaCentro de Estudios Farmacológicos y Botánicos (CEFYBO-CONICET), Serrano 665, Buenos Aires 1414, ArgentinaCentro de Estudios Farmacológicos y Botánicos (CEFYBO-CONICET), Serrano 665, Buenos Aires 1414, ArgentinaCentro de Estudios Farmacológicos y Botánicos (CEFYBO-CONICET), Serrano 665, Buenos Aires 1414, ArgentinaStimulation of phosphoinositide hydrolysis in myocardium from autoimmune myocarditis mice by ThEA and histamine was assayed. Myocardium from autoimmune heart, but not the normal forms, specifically increased phosphoinositide turnover in the presence of histaminergic agonists. This increment was blocked by a specific H1 antagonist mepyramine and to the same extent by the phospholipase C inhibitor NCDC. By using a binding assay H1 histaminergic receptors were detected in autoimmune heart membrane preparations, but this was not observed in normal heart. These data suggest that autoimmune myocardium expressed a functional H1 receptor that could involve a distinctive mechanism operating in the disease.http://dx.doi.org/10.1155/S0962935193000444
collection DOAJ
language English
format Article
sources DOAJ
author Nora Goren
Claudia Perez Leiros
Leonor Sterin-Borda
Enri S. Borda
spellingShingle Nora Goren
Claudia Perez Leiros
Leonor Sterin-Borda
Enri S. Borda
Phosphoinositide hydrolysis mediated by H1 receptors in autoimmune myocarditis mice
Mediators of Inflammation
author_facet Nora Goren
Claudia Perez Leiros
Leonor Sterin-Borda
Enri S. Borda
author_sort Nora Goren
title Phosphoinositide hydrolysis mediated by H1 receptors in autoimmune myocarditis mice
title_short Phosphoinositide hydrolysis mediated by H1 receptors in autoimmune myocarditis mice
title_full Phosphoinositide hydrolysis mediated by H1 receptors in autoimmune myocarditis mice
title_fullStr Phosphoinositide hydrolysis mediated by H1 receptors in autoimmune myocarditis mice
title_full_unstemmed Phosphoinositide hydrolysis mediated by H1 receptors in autoimmune myocarditis mice
title_sort phosphoinositide hydrolysis mediated by h1 receptors in autoimmune myocarditis mice
publisher Hindawi Limited
series Mediators of Inflammation
issn 0962-9351
1466-1861
publishDate 1993-01-01
description Stimulation of phosphoinositide hydrolysis in myocardium from autoimmune myocarditis mice by ThEA and histamine was assayed. Myocardium from autoimmune heart, but not the normal forms, specifically increased phosphoinositide turnover in the presence of histaminergic agonists. This increment was blocked by a specific H1 antagonist mepyramine and to the same extent by the phospholipase C inhibitor NCDC. By using a binding assay H1 histaminergic receptors were detected in autoimmune heart membrane preparations, but this was not observed in normal heart. These data suggest that autoimmune myocardium expressed a functional H1 receptor that could involve a distinctive mechanism operating in the disease.
url http://dx.doi.org/10.1155/S0962935193000444
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AT claudiaperezleiros phosphoinositidehydrolysismediatedbyh1receptorsinautoimmunemyocarditismice
AT leonorsterinborda phosphoinositidehydrolysismediatedbyh1receptorsinautoimmunemyocarditismice
AT enrisborda phosphoinositidehydrolysismediatedbyh1receptorsinautoimmunemyocarditismice
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