Role of alpha- and beta-adrenoreceptors in rat monocyte/macrophage function at rest and acute exercise

• Autores: Juliane da Silva Rossato, Mauricio Krause, Augustus Joli Martins Fernandes, João Roberto Fernandes, Isis Lenhard Seibt, Anderson Rech, Paulo Ivo Homem de Bittencourt Jr.
• Localización: Journal of physiology and biochemistry, ISSN-e 1877-8755, ISSN 1138-7548, Vol. 70, Nº. 2, 2014 (Ejemplar dedicado a: Special Section on the CTP network: Original papers from the 10th meeting of the CTPIOD (Contribution To Progress in Obesity and Diabetes Research), 22th of May 2013, Reus, Spain.), págs. 363-374
• Idioma: inglés
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• Resumen

  • 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 ?- and ?-adrenoreceptors on the function of monocyte/macrophages during rest and exercise. Adult male Wistar rats were i.p. administered (100 ?L/100 g) with specific adrenergic antagonists before an acute moderate exercise bout: prazosin (?1-specific antagonist 2 mg/kg), propranolol (unspecific ?1/?2 antagonist 10 mg/kg), double blockade (?1 and ?1/?2), 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 ?-adrenoreceptor blockade did not change this behavior. In resting animals, ?1 antagonist, as well as the double (?1/?) 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 ?1 stimulation on macrophage activation. In exercised animals, ?1-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 ?- and ?-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 ?1-adrenoreceptor inhibitory tonus that limits macrophage responsiveness but operates differently after physical exercise.