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Fenoterol but not dobutamine increases erythropoietin production in humans
Author(s) -
Gleiter Christoph H.,
Becker Tilmann,
Schreeb Katharina H.,
Freudenthaler Stefan,
GundertRemy Ursula
Publication year - 1997
Publication title -
clinical pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.941
H-Index - 188
eISSN - 1532-6535
pISSN - 0009-9236
DOI - 10.1016/s0009-9236(97)90102-8
Subject(s) - fenoterol , agonist , adrenergic agonist , endocrinology , medicine , erythropoietin , propranolol , chemistry , dobutamine , receptor , pharmacology , hemodynamics , asthma
Objective This study assessed the role of adrenergic signal transmission in the control of renal erythropoietin (EPO) production in humans. Methods Forty‐six healthy male volunteers underwent a hemorrhage of 750 ml. After phlebotomy, they received (intravenously for 6 hours in a parallel, randomized, placebo‐controlled and single‐blind design) either placebo (0.9% sodium chloride), or the β 2 ‐adrenergic receptor agonist fenoterol (1.5 μg/min), or the β 1 ‐adrenergic receptor agonist dobutamine (5 μg/kg/min), or the nonselective β‐adrenergic receptor antagonist propranolol (loading dose of 0.14 mg/kg over 20 minutes, followed by 0.63 μg/kg/min). Results The AUC EPO(0–48hr)fenoterol was 37% higher ( p < 0.03) than AUC EPO(0–48hr)placebo , whereas AUC EPO(0–48hr)dobutamine and AUC EPO(0–48hr)propranolol were comparable with placebo. Creatinine clearance was significantly increased during dobutamine treatment. Urinary cyclic adenosine monophosphate excretion was increased only by fenoterol treatment, whereas serum potassium levels were decreased. Plasma renin activity was significantly increased during dobutamine and fenoterol infusion. Conclusions This study shows in a model of controlled, physiologic stimulation of renal erythropoietin production that the β 2 ‐adrenergic receptor agonist fenoterol but not the β 1 ‐adrenergic receptors agonist dobutamine is able to increase erythropoietin levels in humans. The result can be interpreted as a hint that signals for the control of erythropoietin production may be mediated by β 2 ‐adrenergic receptors rather than by β 1 ‐adrenergic receptors. It appears to be unlikely that an increase of renin concentrations or glomerular filtration rate is causally linked to the control of erythropoietin production in this experimental setting. Clinical Pharmacology & Therapeutics (1997) 61 , 669–676; doi: