title: Role of alpha- and beta-adrenoreceptors in rat monocyte/macrophage function at rest and acute exercise.
abstract: Previous studies from our laboratory have demonstrated that a single bout of moderate exercise stimulates macrophage function, increasing phagocytic capacity, and production of hydrogen peroxide and nitric oxide (NO˙) through nuclear factor kappa B activation. In this work, we investigated the role of α- and β-adrenoreceptors on the function of monocyte/macrophages during rest and exercise. Adult male Wistar rats were i.p. administered (100 μL/100 g) with specific adrenergic antagonists before an acute moderate exercise bout: prazosin (α1-specific antagonist 2 mg/kg), propranolol (unspecific β1/β2 antagonist 10 mg/kg), double blockade (α1 and β1/β2), or phosphate-buffered saline (control). Acute exercise consisted in a single swimming session of moderate intensity (5% body weight overload on the chest) for 60 min. Control groups (rest) received the same antagonists and were killed 60 min after drug administration. Exercise increased phagocytic capacity (1.7-fold, p < 0.05), NO˙ production (5.24 fold, p < 0.001), and inducible nitric oxide synthase (NOS2) expression (by 58.1%), thus suggesting macrophage activation. The β-adrenoreceptor blockade did not change this behavior. In resting animals, α1 antagonist, as well as the double (α1/β) blockade, however, further increased phagocytic capacity (by up to 261%, p < 0.001), NO˙ production (by up to 328%, p < 0.001), and the expressions of NOS2 (by 182%, p < 0.001) and HSP70 (by 42.5%, p < 0.01) suggesting a tonic inhibitory effect of α1 stimulation on macrophage activation. In exercised animals, α1-blockade showed similar enhancing effect on phagocytic indices and expressions of NOS and HSP70, particularly in double-blocked groups, although NO˙ production was found to be reduced in exercised animals submitted to both α- and β-blockade. Redox (glutathione) status and lipoperoxidation were evaluated in all test groups and approximately paralleled macrophage NO˙ production. We suggest the prevalence of a peripheral α1-adrenoreceptor inhibitory tonus that limits macrophage responsiveness but operates differently after physical exercise.
authors.affiliation: Laboratory of Cellular Physiology, Department of Physiology, Institute of Basic Health Sciences, Federal University of Rio Grande do Sul, Rua Sarmento Leite 500 (ICBS), 90050-170, Porto Alegre, Rio Grande do Sul, Brazil.
authors.forename: Juliane
authors.initials: J
authors.lastname: da Silva Rossato
authors.forename: Mauricio
authors.initials: M
authors.lastname: Krause
authors.forename: Augustus Joli Martins
authors.initials: AJ
authors.lastname: Fernandes
authors.forename: João Roberto
authors.initials: JR
authors.lastname: Fernandes
authors.forename: Isis Lenhard
authors.initials: IL
authors.lastname: Seibt
authors.forename: Anderson
authors.initials: A
authors.lastname: Rech
authors.forename: Paulo Ivo
authors.initials: PI
authors.lastname: Homem de Bittencourt
mesh_terms: D058668:Adrenergic alpha-1 Receptor Antagonists / Q000494:pharmacology; D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000818:Animals; D015153:Blotting, Western; D004591:Electrophoresis, Polyacrylamide Gel; D008264:Macrophages / Q000166:cytology*; D008297:Male; D009000:Monocytes / Q000166:cytology*; D010805:Physical Conditioning, Animal; D011224:Prazosin / Q000494:pharmacology; D011433:Propranolol / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D011942:Receptors, Adrenergic, alpha / Q000502:physiology*; D011943:Receptors, Adrenergic, beta / Q000502:physiology*
chemical_list: D058668:Adrenergic alpha-1 Receptor Antagonists; D000319:Adrenergic beta-Antagonists; D011942:Receptors, Adrenergic, alpha; D011943:Receptors, Adrenergic, beta; D011433:Propranolol; D011224:Prazosin