β-Adrenergic and Atrial Natriuretic Peptide Interactions on Human Cardiovascular and Metabolic Regulation
Context: Atrial natriuretic peptide (ANP) has well-known cardiovascular effects and modifies lipid and carbohydrate metabolism in humans. Objective: The objective of the study was to determine the metabolic and cardiovascular interaction of β-adrenergic receptors and ANP. Design: This was a crossove...
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| Published in | The journal of clinical endocrinology and metabolism Vol. 91; no. 12; pp. 5069 - 5075 |
|---|---|
| Main Authors | , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Bethesda, MD
Oxford University Press
01.12.2006
Endocrine Society The Endocrine Society |
| Subjects | |
| Online Access | Get full text |
| ISSN | 0021-972X 1945-7197 |
| DOI | 10.1210/jc.2006-1084 |
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| Abstract | Context: Atrial natriuretic peptide (ANP) has well-known cardiovascular effects and modifies lipid and carbohydrate metabolism in humans.
Objective: The objective of the study was to determine the metabolic and cardiovascular interaction of β-adrenergic receptors and ANP.
Design: This was a crossover study, conducted 2004–2005.
Setting: The study was conducted at an academic clinical research center.
Patients: Patients included 10 healthy young male subjects (body mass index 24 ± 1 kg/m2).
Intervention: We infused iv 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, im, and sc microdialysis and indirect calorimetry. Cardiovascular changes were monitored by continuous electrocardiogram and beat-by-beat blood pressure recordings.
Main Outcome Measures: Venous nonesterified fatty acid, glycerol, glucose, and insulin; and microdialysate glucose, glycerol, lactate, and pyruvate were measured.
Results: ANP increased heart rate dose dependently. β-Adrenergic receptor blockade abolished the response. ANP elicited a dose-dependent increase in serum nonesterified 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, whereas the lactate to pyruvate ratio decreased, both with and without propranolol. Higher ANP doses increased lipid oxidation, whereas energy expenditure remained unchanged. Propranolol tended to attenuate the increase in lipid oxidation.
Conclusions: Selected cardiovascular ANP effects are at least partly mediated by β-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. |
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| AbstractList | Atrial natriuretic peptide (ANP) has well-known cardiovascular effects and modifies lipid and carbohydrate metabolism in humans.
The objective of the study was to determine the metabolic and cardiovascular interaction of beta-adrenergic receptors and ANP.
This was a crossover study, conducted 2004-2005.
The study was conducted at an academic clinical research center.
PATIENTS included 10 healthy young male subjects (body mass index 24 +/- 1 kg/m2).
We infused iv 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, im, and sc microdialysis and indirect calorimetry. Cardiovascular changes were monitored by continuous electrocardiogram and beat-by-beat blood pressure recordings.
Venous nonesterified fatty acid, glycerol, glucose, and insulin; and microdialysate glucose, glycerol, lactate, and pyruvate were measured.
ANP increased heart rate dose dependently. beta-Adrenergic receptor blockade abolished the response. ANP elicited a dose-dependent increase in serum nonesterified 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, whereas the lactate to pyruvate ratio decreased, both with and without propranolol. Higher ANP doses increased lipid oxidation, whereas energy expenditure remained unchanged. Propranolol tended to attenuate the increase in lipid oxidation.
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. CONTEXT: Atrial natriuretic peptide (ANP) has well-known cardiovascular effects and modifies lipid and carbohydrate metabolism in humans. OBJECTIVE: The objective of the study was to determine the metabolic and cardiovascular interaction of beta-adrenergic receptors and ANP. DESIGN: This was a crossover study, conducted 2004-2005. Setting: The study was conducted at an academic clinical research center. Patients: Patients included 10 healthy young male subjects (body mass index 24 +/- 1 kg/m2). INTERVENTION: We infused iv 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, im, and sc microdialysis and indirect calorimetry. Cardiovascular changes were monitored by continuous electrocardiogram and beat-by-beat blood pressure recordings. MAIN OUTCOME MEASURES: Venous nonesterified fatty acid, glycerol, glucose, and insulin; and microdialysate glucose, glycerol, lactate, and pyruvate were measured. RESULTS: ANP increased heart rate dose dependently. beta-Adrenergic receptor blockade abolished the response. ANP elicited a dose-dependent increase in serum nonesterified 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, whereas the lactate to pyruvate ratio decreased, both with and without propranolol. Higher ANP doses increased lipid oxidation, whereas 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. Context: Atrial natriuretic peptide (ANP) has well-known cardiovascular effects and modifies lipid and carbohydrate metabolism in humans. Objective: The objective of the study was to determine the metabolic and cardiovascular interaction of β-adrenergic receptors and ANP. Design: This was a crossover study, conducted 2004–2005. Setting: The study was conducted at an academic clinical research center. Patients: Patients included 10 healthy young male subjects (body mass index 24 ± 1 kg/m2). Intervention: We infused iv 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, im, and sc microdialysis and indirect calorimetry. Cardiovascular changes were monitored by continuous electrocardiogram and beat-by-beat blood pressure recordings. Main Outcome Measures: Venous nonesterified fatty acid, glycerol, glucose, and insulin; and microdialysate glucose, glycerol, lactate, and pyruvate were measured. Results: ANP increased heart rate dose dependently. β-Adrenergic receptor blockade abolished the response. ANP elicited a dose-dependent increase in serum nonesterified 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, whereas the lactate to pyruvate ratio decreased, both with and without propranolol. Higher ANP doses increased lipid oxidation, whereas energy expenditure remained unchanged. Propranolol tended to attenuate the increase in lipid oxidation. Conclusions: Selected cardiovascular ANP effects are at least partly mediated by β-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. Atrial natriuretic peptide (ANP) has well-known cardiovascular effects and modifies lipid and carbohydrate metabolism in humans.CONTEXTAtrial natriuretic peptide (ANP) has well-known cardiovascular effects and modifies lipid and carbohydrate metabolism in humans.The objective of the study was to determine the metabolic and cardiovascular interaction of beta-adrenergic receptors and ANP.OBJECTIVEThe objective of the study was to determine the metabolic and cardiovascular interaction of beta-adrenergic receptors and ANP.This was a crossover study, conducted 2004-2005.DESIGNThis was a crossover study, conducted 2004-2005.The study was conducted at an academic clinical research center.SETTINGThe study was conducted at an academic clinical research center.PATIENTS included 10 healthy young male subjects (body mass index 24 +/- 1 kg/m2).PATIENTSPATIENTS included 10 healthy young male subjects (body mass index 24 +/- 1 kg/m2).We infused iv 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, im, and sc microdialysis and indirect calorimetry. Cardiovascular changes were monitored by continuous electrocardiogram and beat-by-beat blood pressure recordings.INTERVENTIONWe infused iv 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, im, and sc microdialysis and indirect calorimetry. Cardiovascular changes were monitored by continuous electrocardiogram and beat-by-beat blood pressure recordings.Venous nonesterified fatty acid, glycerol, glucose, and insulin; and microdialysate glucose, glycerol, lactate, and pyruvate were measured.MAIN OUTCOME MEASURESVenous nonesterified fatty acid, glycerol, glucose, and insulin; and microdialysate glucose, glycerol, lactate, and pyruvate were measured.ANP increased heart rate dose dependently. beta-Adrenergic receptor blockade abolished the response. ANP elicited a dose-dependent increase in serum nonesterified 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, whereas the lactate to pyruvate ratio decreased, both with and without propranolol. Higher ANP doses increased lipid oxidation, whereas energy expenditure remained unchanged. Propranolol tended to attenuate the increase in lipid oxidation.RESULTSANP increased heart rate dose dependently. beta-Adrenergic receptor blockade abolished the response. ANP elicited a dose-dependent increase in serum nonesterified 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, whereas the lactate to pyruvate ratio decreased, both with and without propranolol. Higher ANP doses increased lipid oxidation, whereas energy expenditure remained unchanged. Propranolol tended to attenuate the increase in lipid oxidation.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.CONCLUSIONSSelected 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. Context: Atrial natriuretic peptide (ANP) has well-known cardiovascular effects and modifies lipid and carbohydrate metabolism in humans. Objective: The objective of the study was to determine the metabolic and cardiovascular interaction of β-adrenergic receptors and ANP. Design: This was a crossover study, conducted 2004–2005. Setting: The study was conducted at an academic clinical research center. Patients: Patients included 10 healthy young male subjects (body mass index 24 ± 1 kg/m2). Intervention: We infused iv 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, im, and sc microdialysis and indirect calorimetry. Cardiovascular changes were monitored by continuous electrocardiogram and beat-by-beat blood pressure recordings. Main Outcome Measures: Venous nonesterified fatty acid, glycerol, glucose, and insulin; and microdialysate glucose, glycerol, lactate, and pyruvate were measured. Results: ANP increased heart rate dose dependently. β-Adrenergic receptor blockade abolished the response. ANP elicited a dose-dependent increase in serum nonesterified 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, whereas the lactate to pyruvate ratio decreased, both with and without propranolol. Higher ANP doses increased lipid oxidation, whereas energy expenditure remained unchanged. Propranolol tended to attenuate the increase in lipid oxidation. Conclusions: Selected cardiovascular ANP effects are at least partly mediated by β-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. |
| Author | Tank, Jens Adams, Frauke Heusser, Karsten Diedrich, André Berlan, Michel Luft, Friedrich C. Boschmann, Michael Lafontan, Max Jordan, Jens Schroeder, Christoph Moro, Cedric Franke, Gabi Birkenfeld, Andreas L. |
| AuthorAffiliation | 1 Franz-Volhard Clinical Research Center Charité Campus Buch and HELIOS Klinikum Berlin,DE 2 Unité de recherche sur les obésités INSERM : U586 IFR31 Université Paul Sabatier - Toulouse III Institut Louis Bugnard Hôpital de Rangueil 1, Avenue Jean Poulhès 31432 TOULOUSE CEDEX 4,FR 3 Autonomic Dysfunction Center, Division of Clinical Pharmacology, Department of Medicine Vanderbilt University Medical School Nashville, Tennesse,US |
| AuthorAffiliation_xml | – name: 3 Autonomic Dysfunction Center, Division of Clinical Pharmacology, Department of Medicine Vanderbilt University Medical School Nashville, Tennesse,US – name: 1 Franz-Volhard Clinical Research Center Charité Campus Buch and HELIOS Klinikum Berlin,DE – name: 2 Unité de recherche sur les obésités INSERM : U586 IFR31 Université Paul Sabatier - Toulouse III Institut Louis Bugnard Hôpital de Rangueil 1, Avenue Jean Poulhès 31432 TOULOUSE CEDEX 4,FR |
| Author_xml | – sequence: 1 givenname: Andreas L. surname: Birkenfeld fullname: Birkenfeld, Andreas L. organization: 1Franz-Volhard Clinical Research Center (A.L.B., M.Bo., F.A., K.H., J.T., C.S., G.F., F.C.L., J.J.), Charité Campus Buch and HELIOS Klinikum, 13125 Berlin, Germany – sequence: 2 givenname: Michael surname: Boschmann fullname: Boschmann, Michael organization: 1Franz-Volhard Clinical Research Center (A.L.B., M.Bo., F.A., K.H., J.T., C.S., G.F., F.C.L., J.J.), Charité Campus Buch and HELIOS Klinikum, 13125 Berlin, Germany – sequence: 3 givenname: Cedric surname: Moro fullname: Moro, Cedric organization: 2Institut National de la Santé et de la Recherche Médicale Unit 586 (C.M., M.Be., M.L.), Institut Louis Bugnard, Université Paul Sabatier, Hôpital Rangueil, 31403 Toulouse, France – sequence: 4 givenname: Frauke surname: Adams fullname: Adams, Frauke organization: 1Franz-Volhard Clinical Research Center (A.L.B., M.Bo., F.A., K.H., J.T., C.S., G.F., F.C.L., J.J.), Charité Campus Buch and HELIOS Klinikum, 13125 Berlin, Germany – sequence: 5 givenname: Karsten surname: Heusser fullname: Heusser, Karsten organization: 1Franz-Volhard Clinical Research Center (A.L.B., M.Bo., F.A., K.H., J.T., C.S., G.F., F.C.L., J.J.), Charité Campus Buch and HELIOS Klinikum, 13125 Berlin, Germany – sequence: 6 givenname: Jens surname: Tank fullname: Tank, Jens organization: 1Franz-Volhard Clinical Research Center (A.L.B., M.Bo., F.A., K.H., J.T., C.S., G.F., F.C.L., J.J.), Charité Campus Buch and HELIOS Klinikum, 13125 Berlin, Germany – sequence: 7 givenname: André surname: Diedrich fullname: Diedrich, André organization: 3Autonomic Dysfunction Center (A.D.), Division of Clinical Pharmacology, Department of Medicine, Vanderbilt University Medical School, Nashville, Tennessee 37232 – sequence: 8 givenname: Christoph surname: Schroeder fullname: Schroeder, Christoph organization: 1Franz-Volhard Clinical Research Center (A.L.B., M.Bo., F.A., K.H., J.T., C.S., G.F., F.C.L., J.J.), Charité Campus Buch and HELIOS Klinikum, 13125 Berlin, Germany – sequence: 9 givenname: Gabi surname: Franke fullname: Franke, Gabi organization: 1Franz-Volhard Clinical Research Center (A.L.B., M.Bo., F.A., K.H., J.T., C.S., G.F., F.C.L., J.J.), Charité Campus Buch and HELIOS Klinikum, 13125 Berlin, Germany – sequence: 10 givenname: Michel surname: Berlan fullname: Berlan, Michel organization: 2Institut National de la Santé et de la Recherche Médicale Unit 586 (C.M., M.Be., M.L.), Institut Louis Bugnard, Université Paul Sabatier, Hôpital Rangueil, 31403 Toulouse, France – sequence: 11 givenname: Friedrich C. surname: Luft fullname: Luft, Friedrich C. organization: 1Franz-Volhard Clinical Research Center (A.L.B., M.Bo., F.A., K.H., J.T., C.S., G.F., F.C.L., J.J.), Charité Campus Buch and HELIOS Klinikum, 13125 Berlin, Germany – sequence: 12 givenname: Max surname: Lafontan fullname: Lafontan, Max organization: 2Institut National de la Santé et de la Recherche Médicale Unit 586 (C.M., M.Be., M.L.), Institut Louis Bugnard, Université Paul Sabatier, Hôpital Rangueil, 31403 Toulouse, France – sequence: 13 givenname: Jens surname: Jordan fullname: Jordan, Jens email: jordan@fvk.charite-buch.de organization: 1Franz-Volhard Clinical Research Center (A.L.B., M.Bo., F.A., K.H., J.T., C.S., G.F., F.C.L., J.J.), Charité Campus Buch and HELIOS Klinikum, 13125 Berlin, Germany |
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| Copyright | Copyright © 2006 by The Endocrine Society 2006 2007 INIST-CNRS Copyright © 2006 by The Endocrine Society Distributed under a Creative Commons Attribution 4.0 International License |
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| Issue | 12 |
| Keywords | Human Regulation(control) Natriuretic hormone Atrial natriuretic peptide Circulatory system Metabolism Endocrinology β-Adrenergic receptor |
| Language | English |
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| Snippet | Context: Atrial natriuretic peptide (ANP) has well-known cardiovascular effects and modifies lipid and carbohydrate metabolism in humans.
Objective: The... Atrial natriuretic peptide (ANP) has well-known cardiovascular effects and modifies lipid and carbohydrate metabolism in humans. The objective of the study was... Context: Atrial natriuretic peptide (ANP) has well-known cardiovascular effects and modifies lipid and carbohydrate metabolism in humans. Objective: The... Atrial natriuretic peptide (ANP) has well-known cardiovascular effects and modifies lipid and carbohydrate metabolism in humans.CONTEXTAtrial natriuretic... CONTEXT: Atrial natriuretic peptide (ANP) has well-known cardiovascular effects and modifies lipid and carbohydrate metabolism in humans. OBJECTIVE: The... |
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| SubjectTerms | Adipose Tissue Adipose Tissue - cytology Adipose Tissue - drug effects Adrenergic beta-Antagonists Adrenergic beta-Antagonists - pharmacology Adrenergic receptors Adult Atrial Natriuretic Factor Atrial Natriuretic Factor - administration & dosage Atrial Natriuretic Factor - pharmacology Atrial Natriuretic Factor - physiology Atrial natriuretic peptide Biological and medical sciences Blood Glucose Blood Glucose - analysis Blood pressure Body mass index Calorimetry Calorimetry, Indirect Carbohydrate metabolism Cardiology and cardiovascular system Cardiovascular Physiological Phenomena Cardiovascular Physiology Cells, Cultured Dose-Response Relationship, Drug EKG Endocrinopathies Energy expenditure Fatty acids Fatty Acids, Nonesterified Fatty Acids, Nonesterified - blood Female Fundamental and applied biological sciences. Psychology Glucose Glucose - metabolism Glycerol Glycerol - blood Glycerol - metabolism Glycolysis Heart Heart rate Heart Rate - drug effects Human health and pathology Humans Infusions, Intravenous Insulin Lactic acid Life Sciences Lipid metabolism Lipid peroxidation Lipids Male Medical sciences Metabolism Microdialysis Muscle, Skeletal - drug effects Oxidation Peptides Propranolol Propranolol - pharmacology Pyruvic acid Receptors, Adrenergic, beta - physiology Skeletal muscle Vertebrates: endocrinology |
| Title | β-Adrenergic and Atrial Natriuretic Peptide Interactions on Human Cardiovascular and Metabolic Regulation |
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