| http://purl.uniprot.org/citations/17911346 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/17911346 | http://www.w3.org/2000/01/rdf-schema#comment | "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."xsd:string |
| http://purl.uniprot.org/citations/17911346 | http://purl.org/dc/terms/identifier | "doi:10.1152/ajpendo.00288.2007"xsd:string |
| http://purl.uniprot.org/citations/17911346 | http://purl.uniprot.org/core/author | "Lakatta E.G."xsd:string |
| http://purl.uniprot.org/citations/17911346 | http://purl.uniprot.org/core/author | "Spencer R.G."xsd:string |
| http://purl.uniprot.org/citations/17911346 | http://purl.uniprot.org/core/author | "McConville P."xsd:string |
| http://purl.uniprot.org/citations/17911346 | http://purl.uniprot.org/core/date | "2007"xsd:gYear |
| http://purl.uniprot.org/citations/17911346 | http://purl.uniprot.org/core/name | "Am J Physiol Endocrinol Metab"xsd:string |
| http://purl.uniprot.org/citations/17911346 | http://purl.uniprot.org/core/pages | "E1828-35"xsd:string |
| http://purl.uniprot.org/citations/17911346 | http://purl.uniprot.org/core/title | "Greater glycogen utilization during 1- than 2-adrenergic receptor stimulation in the isolated perfused rat heart."xsd:string |
| http://purl.uniprot.org/citations/17911346 | http://purl.uniprot.org/core/volume | "293"xsd:string |
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