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Titolo:
Comparison of the electromechanical responsiveness of alpha-1-adrenoceptorstimulation in ventricles of normal and cardiomyopathic hamsters
Autore:
Chen, WP; Su, MJ;
Indirizzi:
Natl Taiwan Univ, Coll Med, Inst Pharmacol, Taipei 100, Taiwan Natl TaiwanUniv Taipei Taiwan 100 d, Inst Pharmacol, Taipei 100, Taiwan
Titolo Testata:
JOURNAL OF BIOMEDICAL SCIENCE
fascicolo: 6, volume: 8, anno: 2001,
pagine: 453 - 461
SICI:
1021-7770(200111/12)8:6<453:COTERO>2.0.ZU;2-5
Fonte:
ISI
Lingua:
ENG
Soggetto:
ACTION-POTENTIAL PROLONGATION; HEART-FAILURE; SARCOPLASMIC-RETICULUM; SYRIAN-HAMSTERS; CARDIAC MYOCYTES; SIGNAL-TRANSDUCTION; CALCIUM; PROTEIN; MYOCARDIUM; MECHANISMS;
Keywords:
alpha(1)-adrenoceptor; phenylephrine; protein kinase C; cardiomyopathic BIO 14.6 hamster;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
38
Recensione:
Indirizzi per estratti:
Indirizzo: Su, MJ Natl Taiwan Univ, Coll Med, Inst Pharmacol, 1,Sec 1 Jen Ai Rd, Taipei 100,Taiwan Natl Taiwan Univ 1,Sec 1 Jen Ai Rd Taipei Taiwan 100 ei 100,Taiwan
Citazione:
W.P. Chen e M.J. Su, "Comparison of the electromechanical responsiveness of alpha-1-adrenoceptorstimulation in ventricles of normal and cardiomyopathic hamsters", J BIOMED SC, 8(6), 2001, pp. 453-461

Abstract

Alterations in alpha (1)-adrenoceptor (alpha (1)AR) density and related signal transduction proteins were reported in cardiomyopathic hearts in the failing stage. The electromechanical modification of alpha (1)-adrenergic stimulation in the failing heart is unclear. The present study compares the alpha (1)AR-stimulated electromechanical response in failing ventricles of genetically cardiomyopathic BIO 14.6 hamsters (280-320 days old) with that in age-matched normal Syrian hamsters. The action potential was recorded with a conventional microelectrode technique, and twitch force was measured with a transducer. In the presence of propranolol, phenylephrine increased the contraction and prolonged the action potential duration (APD) to similar values in ventricles of both strains, despite a prolonged basal APD in cardiormyopathic ventricles. The positive inotropism stimulated by phenylephrine was inhibited by staurosporine, and was potentiated by 4 beta -phorbol-12,13-dibutyrate (PDBu) in both strains. The maximum positive inotropic effect of phenylephrine in PDBu-treated ventricles of normal hamsters was significantly greater than that in BIO 14.6 hamsters. The effects of phenylephrine on the ventricular force-frequency relationship and on the mechanical restitution in both nor-mall and BIO 14.6 strain hamsters were examined. The uniform negative force-frequency relationship and the altered mechanical restitution reveal a defect of intracellular Ca2+ handling in cardiomyopathic BIO 14.6 hamsters. alpha (1)-Adrenergic modulation cannot convert the defective properties in the model of the failing heart. Nevertheless, phenylephrine decreased postrest potentiation in short rest periods, and enhanced postrest decay after longer resting periods. The results indicate that alpha (1-)adrenergic action enhances a gradual loss of Ca2+ from the sarcoplasmic reticulum, although its action in prolonging the APD can indirectly increase the influx of Ca2+. Copyright (C) 2001 National Science Council, ROC and S. Karger AG, Basel.

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Documento generato il 31/03/20 alle ore 09:24:53