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Beta-adrenergic and atrial natriuretic peptide interactions on human cardiovascular and metabolic regulation

Item Type:Article
Title:Beta-adrenergic and atrial natriuretic peptide interactions on human cardiovascular and metabolic regulation
Creators Name:Birkenfeld, A.L. and Boschmann, M. and Moro, C. and Adams, F. and Heusser, K. and Tank, J. and Diedrich, A. and Schroeder, C. and Franke, G. and Berlan, M. and Luft, F.C. and Lafontan, M. and Jordan, J.
Abstract:CONTEXT: Atrial natriuretic peptide (ANP) has well known cardiovascular effects and modifies lipid and carbohydrate metabolism in humans. OBJECTIVE: To determine the metabolic and cardiovascular interaction of beta-adrenergic receptors and ANP. DESIGN: Cross over study, conducted 2004-2005 Setting: Academic clinical research center PATIENTS: Ten healthy, young, male subjects (BMI 24 +/- 1 kg/m(2)) INTERVENTION: We infused intravenously incremental ANP doses (6.25, 12.5, and 25 ng/kg/min) with and without propranolol (0.20 mg/kg in divided doses followed by 0.033 mg/kg/h infusion). Metabolism was monitored through venous blood sampling, intramuscular and sc microdialysis and indirect calorimetry. Cardiovascular changes where monitored by continuous ECG and beat-by-beat blood pressure recordings. MAIN OUTCOME MEASURES: Venous NEFA, glycerol, glucose, insulin, microdialysate glucose, glycerol, lactate, pyruvate. RESULTS: ANP increased heart rate dose dependently. beta-adrenergic receptor blockade abolished the response. ANP elicited a dose-dependent increase in serum non-esterified fatty acid and glycerol concentrations. The response was not suppressed with propranolol. Venous glucose and insulin concentrations increased with ANP, both, without or with propranolol. ANP induced lipid mobilization in sc adipose tissue. In skeletal muscle, microdialysate lactate increased while the lactate to pyruvate ratio decreased, both, with and without propranolol. Higher ANP doses increased lipid oxidation while energy expenditure remained unchanged. Propranolol tended to attenuate the increase in lipid oxidation. CONCLUSIONS: Selected cardiovascular ANP effects are at least partly mediated by beta-adrenergic receptor stimulation. ANP induced changes in lipid mobilization and glycolysis are mediated by another mechanism, presumably stimulation of natriuretic peptide receptors whereas substrate oxidation might be modulated through adrenergic mechanisms.
Keywords:Adipose Tissue, Adrenergic beta-Antagonists, Atrial Natriuretic Factor, Blood Glucose, Beta Adrenergic Receptors, Cardiovascular Physiological Phenomena, Cultured Cells, Drug Dose-Response Relationship, Glucose, Glycerol, Heart Rate, Indirect Calorimetry, Intravenous Infusions, Metabolism, Microdialysis, Nonesterified Fatty Acids, Propranolol, Skeletal Muscle
Source:Journal of Clinical Endocrinology and Metabolism
Publisher:Endocrine Society
Page Range:5069-5075
Date:December 2006
Official Publication:https://doi.org/10.1210/jc.2006-1084
PubMed:View item in PubMed

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