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

Authors

  • A.L. Birkenfeld
  • M. Boschmann
  • C. Moro
  • F. Adams
  • K. Heusser
  • J. Tank
  • A. Diedrich
  • C. Schroeder
  • G. Franke
  • M. Berlan
  • F.C. Luft
  • M. Lafontan
  • J. Jordan

Journal

  • Journal of Clinical Endocrinology and Metabolism

Citation

  • J Clin Endocrinol Metab 91 (12): 5069-5075

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.


DOI

doi:10.1210/jc.2006-1084