Kappa-opioid Receptor Stimulation Inhibits Cardiac Hypertrophy Induced by Beta1-adrenoceptor Stimulation in the Rat.
From: Key Lab of Molecular Biology and Drug Research, Jinzhou Medical College, Jinzhou, China.
European journal of pharmacology
- Publish Date: Jan 2007
- ISSN: 0014-2999
- Volume: 555
- Issue: 2-3
- Pages: 100-5
- Medium: Print
- Language: English
- Citation (JAMA): Shan Dan, Wang Hongxin, Su Yuhong, et al. Kappa-opioid Receptor Stimulation Inhibits Cardiac Hypertrophy Induced by Beta1-adrenoceptor Stimulation in the Rat.. Eur. J. Pharmacol. Jan 2007;555:100-5
Abstract
To test the hypothesis that kappa-opioid receptor stimulation inhibits cardiac hypertrophy induced by beta1-adrenoceptor stimulation, we determined the effects of trans-(+/-)-3,4-dichloro-N-methyl-N-[2-(1-pyrrolidinyl)-cyclohexyl]-benzeneacetamide methanesulfonate salt (U50,488H), a selective kappa-opioid receptor agonist, on cardiac hypertrophy induced by isoprenaline, a selective beta-adrenoceptor agonist, in neonatal ventricular myocytes upon blockade of beta2-adrenoceptor. Hypertrophy of cardiomyocytes was determined by increases in (i) total protein content; (ii) [3H]leucine incorporation; and iii) cell size. 10 micromol/l isoprenaline increased all three parameters. The effects were abolished by 2 micromol/l propranolol, a beta-adrenergic receptor antagonist, or 300 nmol/l CGP20712A, a beta1-adrenoceptor antagonist, but not by 100 nmol/l ICI118,551, a beta2-adrenoceptor antagonist. The effects were also abolished by Rp-cAMPs 100 micromol/l, a protein kinase A inhibitor and not by pertussis toxin 5 mg/l. The effects of isoprenaline in the presence or absence of ICI118,551 were also abolished by 1 micromol/l U50,488H. The inhibitory effects of U50,488H were abolished by 1 micromol/l nor-binaltorphimine, a selective kappa-opioid receptor antagonist. U50,488H also abolished the increases in the amplitude and frequency of the spontaneous intracellular Ca2+ transient induced by 10 micromol/l isoprenaline in the presence or absence of ICI118,551, an effect also abolished by nor-binaltorphimine. In conclusion the results show that kappa-opioid receptor stimulation abolished both the cardiac hypertrophy and enhanced amplitude and frequency of the spontaneous intracellular Ca2+ transient induced by beta1-adrenoceptor stimulation.
Mesh Headings (Keywords): 3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, (trans)-Isomer, Adrenergic beta-Agonists, Adrenergic beta-Antagonists, Animals, Animals, Newborn, Calcium, Cardiomegaly, Cell Size, Cells, Cultured, Imidazoles, Isoproterenol, Leucine, Myocytes, Cardiac, Propanolamines, Proteins, Rats, Rats, Sprague-Dawley, Receptors, Adrenergic, beta-1, Receptors, Adrenergic, beta-2, Receptors, Opioid, kappa
Check for Full Text / PubMed Unique Identifier (PMID): 17126321
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