β-Agonist stimulation produces changes in cardiac AMPK and coronary lumen LPL only during increased workload
| Autor: | Ashraf Abrahani, Ding An, Girsh Kewalramani, Brian Rodrigues, Sheila M. Innis, Rich Wambolt, Sanjoy Ghosh, Michael F. Allard, Dake Qi, Thomas Pulinilkunnil |
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| Rok vydání: | 2005 |
| Předmět: |
Male
Agonist Langendorff heart medicine.medical_specialty Endothelium Physiology medicine.drug_class Endocrinology Diabetes and Metabolism Blotting Western Lumen (anatomy) AMP-Activated Protein Kinases In Vitro Techniques Protein Serine-Threonine Kinases AMP-activated protein kinase Multienzyme Complexes Physical Conditioning Animal Physiology (medical) Internal medicine medicine Animals Myocytes Cardiac Phosphorylation Rats Wistar Lipoprotein lipase biology Reverse Transcriptase Polymerase Chain Reaction Myocardium Isoproterenol AMPK Heart Adrenergic beta-Agonists Myocardial Contraction Stimulation Chemical Rats Lipoprotein Lipase Endocrinology medicine.anatomical_structure Circulatory system biology.protein RNA Endothelium Vascular Acetyl-CoA Carboxylase |
| Zdroj: | American Journal of Physiology-Endocrinology and Metabolism. 288:E1120-E1127 |
| ISSN: | 1522-1555 0193-1849 |
| DOI: | 10.1152/ajpendo.00588.2004 |
| Popis: | Given the importance of lipoprotein lipase (LPL) in cardiac and vascular pathology, the objective of the present study was to investigate whether the β-agonist isoproterenol (Iso) influences cardiac LPL. Incubation of quiescent cardiomyocytes with Iso for 60 min had no effect on basal, intracellular, or heparin-releasable (HR)-LPL activity. Similarly, Iso did not change HR-LPL in Langendorff isolated hearts that do not beat against an afterload. In the intact animal, LPL activity at the vascular lumen increased significantly in the Iso-treated group, together with a substantial increase in rate-pressure product. This LPL increase was likely via mechanisms regulated by activation of AMP-activated protein kinase (AMPK) and inactivation of acetyl-CoA carboxylase (ACC280). In glucose-perfused hearts, simply switching from Langendorff to the isolated working heart (that beats against an afterload) induced increases in AMPK and ACC280phosphorylation and enhanced HR-LPL activity. Provision of insulin and albumin-bound palmitic acid to the working heart was able to reverse these effects. In these hearts, introduction of Iso to the buffer perfusate duplicated the effects seen when this β-agonist was given in vivo. Our data suggest that Iso can influence HR-LPL only during conditions of increased workload, mechanical performance and excessive energy expenditure, and likely in an AMPK-dependent manner. |
| Databáze: | OpenAIRE |
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