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Greater glycogen utilization during 1- than 2-adrenergic receptor stimulation in the isolated perfused rat heart.

Authors: McConville, P  Lakatta, EG  Spencer, RG 
Citation: McConville P, etal., Am J Physiol Endocrinol Metab. 2007 Dec;293(6):E1828-35. Epub 2007 Oct 2.
Pubmed: (View Article at PubMed) PMID:17911346
DOI: Full-text: DOI:10.1152/ajpendo.00288.2007

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.

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CRRD Object Information
CRRD ID: 5129142
Created: 2011-03-24
Species: All species
Last Modified: 2011-03-24
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.