Document Detail


Influence of atenolol and nifedipine on nitric-oxide deficient cardiomyocyte hypertrophy and expression of the cardio-endocrine peptide intermedin and its receptor components.
MedLine Citation:
PMID:  18209487     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND/AIMS: Chronic inhibition of nitric oxide (NO) synthesis is associated with hypertension, myocardial ischemia, oxidative stress and hypertrophy; expression of adrenomedullin (AM) and intermedin (IMD) and their receptor activity modifying proteins (RAMPs 1-3) is augmented in cardiomyocytes, indicating that the myocardial AM/ IMD system may be activated in response to pressure loading and ischemic insult. The aim was to examine effects on (i) parameters of cardiomyocyte hypertrophy and on (ii) expression of AM and IMD and their receptor components in NO-deficient cardiomyocytes of an intervention chosen specifically for ability to alleviate pressure loading and ischemic injury concurrently.
METHODS: The NO synthesis inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME, 35 mg.kg(-1).day(-1)) was given to rats for 8 weeks, with/ without concurrent administration of beta-adrenoceptor antagonist, atenolol (25 mg.kg(-1).day(-1)) / calcium channel blocker, nifedipine (20mg.kg(-1).day(-1)).
RESULTS: In L-NAME treated rats, atenolol / nifedipine abolished increases in systolic blood pressure and plasma AM and IMD levels and in left ventricular cardiomyocytes: (i) normalized increased cell width and mRNA expression of hypertrophic (sk-alpha-actin) and cardio-endocrine (ANP, BNP, ET) genes; (ii) normalized augmented membrane protein oxidation; (iii) normalized mRNA expression of AM, IMD, RAMP1, RAMP2 and RAMP3.
CONCLUSIONS: normalization of blood pressure and membrane oxidant status together with prevention of hypertrophy and normalization of the augmented expression of AM, IMD and their receptor components in NO-deficient cardiomyocytes by atenolol / nifedipine supports involvement of both pressure loading and ischemic insult in stimulating cardiomyocyte hypertrophy and induction of these counter-regulatory peptides and their receptor components. Attenuation of augmented expression of IMD in this model cannot however be explained simply by prevention of cardiomyocyte hypertrophy.
Authors:
David Bell; You You Zhao; Adrian B Devine; Barbara J McDermott
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2008-01-17
Journal Detail:
Title:  Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology     Volume:  21     ISSN:  1015-8987     ISO Abbreviation:  Cell. Physiol. Biochem.     Publication Date:  2008  
Date Detail:
Created Date:  2008-01-22     Completed Date:  2008-03-26     Revised Date:  2010-12-01    
Medline Journal Info:
Nlm Unique ID:  9113221     Medline TA:  Cell Physiol Biochem     Country:  Switzerland    
Other Details:
Languages:  eng     Pagination:  203-14     Citation Subset:  IM    
Affiliation:
Cardiovascular Research Group, Division of Medicine and Therapeutics, School of Medicine and Dentistry, The Queen's University of Belfast, Belfast, Northern Ireland, UK. d.bell@qub.ac.uk
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MeSH Terms
Descriptor/Qualifier:
Adrenomedullin / blood,  genetics,  metabolism*
Animals
Atenolol / pharmacology*
Atrial Natriuretic Factor / genetics,  metabolism
Blood Pressure / drug effects
Endothelin-1 / genetics,  metabolism
Gene Expression Regulation / drug effects
Hypertrophy
Intracellular Signaling Peptides and Proteins / genetics,  metabolism
Male
Membrane Proteins / genetics,  metabolism
Myocytes, Cardiac / drug effects*,  metabolism,  pathology*
NG-Nitroarginine Methyl Ester / administration & dosage,  pharmacology
Natriuretic Peptide, Brain / genetics,  metabolism
Neuropeptides / blood,  genetics,  metabolism*
Nifedipine / pharmacology*
Nitric Oxide / deficiency*
Oxidative Stress / drug effects
Peptides / genetics,  metabolism
Protein Precursors / genetics,  metabolism
Rats
Rats, Sprague-Dawley
Receptor Activity-Modifying Protein 1
Receptor Activity-Modifying Protein 3
Receptor Activity-Modifying Proteins
Receptors, Cell Surface / genetics,  metabolism*
Systole / drug effects
Chemical
Reg. No./Substance:
0/Endothelin-1; 0/Intracellular Signaling Peptides and Proteins; 0/Membrane Proteins; 0/Neuropeptides; 0/Peptides; 0/Protein Precursors; 0/Ramp1 protein, rat; 0/Ramp2 protein, rat; 0/Ramp3 protein, rat; 0/Receptor Activity-Modifying Protein 1; 0/Receptor Activity-Modifying Protein 3; 0/Receptor Activity-Modifying Proteins; 0/Receptors, Cell Surface; 0/intermedin protein, rat; 10102-43-9/Nitric Oxide; 114471-18-0/Natriuretic Peptide, Brain; 148498-78-6/Adrenomedullin; 21829-25-4/Nifedipine; 29122-68-7/Atenolol; 50903-99-6/NG-Nitroarginine Methyl Ester; 85637-73-6/Atrial Natriuretic Factor

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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