UM
Crosstalk between alpha-1A and alpha-1B adrenoceptors in neonatal rat myocardium: Implications in cardiac hypertrophy
Deng X.-F.1; Sculptoreanu A.2; Mulay S.1; Peri K.G.3; Li J.-F.1; Zheng W.-H.1; Chemtob S.1; Varma D.R.1
1998-07-01
Source PublicationJournal of Pharmacology and Experimental Therapeutics
ISSN00223565
Volume286Issue:1Pages:489-496
AbstractThe myocardial effects of alpha-1A adrenoceptor (alpha-1 AR) agonists in neonatal rats are mediated by alpha-1A AR and not by alpha-1B AR, although both receptor subtypes are equally expressed; the functions of alpha-1B AR are not known. Here, we report that alpha-1B ARs inhibit the activities of alpha-1A ARs in neonatal rat myocardium so that the inactivation of alpha-1B ARs by chloroethylclonidine (CEC) potentiated the effects of nonselective alpha-1 AR agonist phenylephrine (PE) on myocardial protein synthesis and early gene (c-fos and c-jun) expression. CEC did not modify the hypertrophic effect of angiotensin II. The potentiation of the effects of PE by CEC was associated with a translocation of Ca-dependent protein kinase C (PKC)α, which did not occur in the absence of CEC. Alpha-1A AR-selective agonist A61603 was ~1000-fold more potent than PE as a positive inotropic agent; it caused the translocation of PKCα, which was not affected by CEC. 5- Methylurapidil antagonized the effects of PE and A61603, suggesting that these were mediated via alpha-1A ARs. Alpha-1D AR antagonist BMY 7378 did not modify PE-induced translocation of PKC. CEC potentiated the effects of PE on Ca transients in Fura 2-AM-loaded dispersed cardiomyocytes, and this potentiation was prevented by nifedipine. In whole-cell patch-clamp recordings of cultured cardiomyocytes, CEC potentiated the effect of norepinephrine on Ca channel currents, which was blocked by 5- methylurapidil. We conclude that alpha-1A ARs are positively and alpha-1B ARs are negatively coupled to nifedipine-sensitive Ca channels, possibly via G(i) protein, and this antagonistic relationship between alpha-A AR and alpha-1B AR in the neonatal heart might be required physiologically for normal alpha-1 AR-mediated responses and myocardial development.
URLView the original
Language英語
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Document TypeJournal article
专题University of Macau
Affiliation1.McGill University
2.Lady Davis Institute for Medical Research
3.CHU Sainte-Justine - Le centre hospitalier universitaire mère-enfant
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Deng X.-F.,Sculptoreanu A.,Mulay S.,et al. Crosstalk between alpha-1A and alpha-1B adrenoceptors in neonatal rat myocardium: Implications in cardiac hypertrophy[J]. Journal of Pharmacology and Experimental Therapeutics,1998,286(1):489-496.
APA Deng X.-F..,Sculptoreanu A..,Mulay S..,Peri K.G..,Li J.-F..,...&Varma D.R..(1998).Crosstalk between alpha-1A and alpha-1B adrenoceptors in neonatal rat myocardium: Implications in cardiac hypertrophy.Journal of Pharmacology and Experimental Therapeutics,286(1),489-496.
MLA Deng X.-F.,et al."Crosstalk between alpha-1A and alpha-1B adrenoceptors in neonatal rat myocardium: Implications in cardiac hypertrophy".Journal of Pharmacology and Experimental Therapeutics 286.1(1998):489-496.
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