Document Detail


Greater glycogen utilization during 1- than 2-adrenergic receptor stimulation in the isolated perfused rat heart.
MedLine Citation:
PMID:  17911346     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Differences in energy metabolism during beta(1)- and beta(2)-adrenergic receptor (AR) stimulation have been shown to translate to differences in the elicited functional responses. It has been suggested that differential access to glycogen during beta(1)- compared with beta(2)-AR stimulation may influence the peak functional response and modulation of the response during sustained adrenergic stimulation. Interleaved (13)C- and (31)P-NMR spectroscopy was used during beta(1)- and beta(2)-AR stimulation at matched peak workload (2.5 times baseline) in the isolated perfused rat heart to monitor glycogen levels, phosphorylation potential, and intracellular pH. Simultaneous measurements of left ventricular (LV) function [LV developed pressure (LVDP)], heart rate (HR), and rate-pressure product (RPP = LVDP x HR) were also performed. The heart was perfused under both substrate-free (SF) conditions and with exogenous glucose (G). The greater glycogenolysis was observed during beta(1)- than beta(2)-AR stimulation with G (54% vs. 38% reduction, P = 0.006) and SF (92% vs. 79% reduction, P = 0.04) perfusions. The greater beta(1)-AR-mediated glycogenolysis was correlated with greater ability to sustain the initial contractile response. However, with SF perfusion, the duration of this ability was limited: excessive early glycogen depletion caused an earlier decline in LVDP and phosphorylation potential during beta(1)- than beta(2)-AR stimulation. Therefore, endogenous glycogen stores are depleted earlier and to a greater extent, despite a slightly weaker overall inotropic response, during beta(1)- than beta(2)-AR stimulation. These findings are consistent with beta(1)-AR-specific PKA-dependent glycogen phosphorylase kinase signaling.
Authors:
Patrick McConville; Edward G Lakatta; Richard G Spencer
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Publication Detail:
Type:  In Vitro; Journal Article; Research Support, N.I.H., Intramural     Date:  2007-10-02
Journal Detail:
Title:  American journal of physiology. Endocrinology and metabolism     Volume:  293     ISSN:  0193-1849     ISO Abbreviation:  Am. J. Physiol. Endocrinol. Metab.     Publication Date:  2007 Dec 
Date Detail:
Created Date:  2007-12-10     Completed Date:  2008-02-25     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  100901226     Medline TA:  Am J Physiol Endocrinol Metab     Country:  United States    
Other Details:
Languages:  eng     Pagination:  E1828-35     Citation Subset:  IM    
Affiliation:
Laboratory of Clinical Investigation, Box 29, Gerontology Research Center 4D-08, 5600 Nathan Shock Dr., Baltimore, MD 21 224, USA.
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MeSH Terms
Descriptor/Qualifier:
Adrenergic alpha-Agonists / pharmacology
Adrenergic alpha-Antagonists / pharmacology
Adrenergic beta-Agonists / pharmacology
Adrenergic beta-Antagonists / pharmacology
Animals
Bisoprolol / pharmacology
Ethanolamines / pharmacology
Glucose / pharmacology
Glycogen / metabolism*
Glycogenolysis / drug effects,  physiology
Heart / drug effects,  physiology
Heart Rate / drug effects
Magnetic Resonance Spectroscopy
Male
Models, Biological
Myocardium / metabolism*
Norepinephrine / pharmacology
Perfusion
Phosphocreatine / metabolism
Prazosin / pharmacology
Rats
Rats, Wistar
Receptors, Adrenergic, beta-1 / agonists,  antagonists & inhibitors,  physiology*
Receptors, Adrenergic, beta-2 / agonists,  antagonists & inhibitors,  physiology*
Ventricular Function, Left / drug effects
Chemical
Reg. No./Substance:
0/Adrenergic alpha-Agonists; 0/Adrenergic alpha-Antagonists; 0/Adrenergic beta-Agonists; 0/Adrenergic beta-Antagonists; 0/Ethanolamines; 0/Receptors, Adrenergic, beta-1; 0/Receptors, Adrenergic, beta-2; 19216-56-9/Prazosin; 37000-20-7/zinterol; 50-99-7/Glucose; 51-41-2/Norepinephrine; 66722-44-9/Bisoprolol; 67-07-2/Phosphocreatine; 9005-79-2/Glycogen

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


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