Chronic propranolol treatment affects expression of adrenoceptors on peritoneal macrophages and their ability to produce hydrogen peroxide and nitric oxide
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2009
Authors
Dimitrijević, MirjanaPilipović, Ivan
Stanojević, Stanislava
Mitić, Katarina
Radojević, Katarina
Pešić, Vesna
Leposavić, Gordana
Article (Published version)
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Using both immunocytochemical and flow cytometric analyses of rat peritoneal exudate cells constitutive expression of tyrosine hydroxylase and both beta(2)- and alpha(1)-adrenoceptors on macrophages was revealed. Furthermore, according to the characteristic assemblage of tyrosine hydroxylase and adrenoceptor subtype expression different macrophage subsets were identified. In vitro treatment of macrophages with the nonselective alpha,beta-adrenoceptor agonist arterenol and/or the beta-adrenoceptor antagonist propranolol indicated that beta-adrenoceptors potentiated nitric oxide (NO) production and suggested alpha-adrenoceptor-mediated suppression of hydrogen peroxide (H2O2) production. An increase in H2O2 production in the presence of the alpha(1)-adrenoceptor antagonist ebrantil provided support for this. Chronic propranolol treatment in vivo led to increased NO and H2O2 production by peritoneal macrophages. Furthermore, this treatment resulted in opposing effects on the expression Of ...beta(2)- and alpha(1)-adrenoceptors on peritoneal macrophages (a stimulatory effect on beta(2)-adrenoceptors and a suppressive effect on alpha(1)-adrenoceptors). In conclusion, a subset of resident peritoneal macrophages synthesizes catecholamines, which may exert differential effects on H2O2 and NO production via distinct adrenoceptors. Finally, chronic propranolol treatment affected adrenoceptor expression on peritoneal macrophages and altered their capacity to generate NO and H2O2.
Keywords:
alpha-adrenoceptor / beta-adrenoceptor / Catecholamines / Macrophages / RatSource:
Journal of Neuroimmunology, 2009, 211, 1-2, 56-65Publisher:
- Elsevier Science BV, Amsterdam
Funding / projects:
- Neuroendokrina modulacija imunskog odgovora: uloga simpato-adrenomedularnog sistema (RS-MESTD-MPN2006-2010-145049)
DOI: 10.1016/j.jneuroim.2009.03.014
ISSN: 0165-5728
PubMed: 19398131
WoS: 000268035000006
Scopus: 2-s2.0-67349256113
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Institution/Community
PharmacyTY - JOUR AU - Dimitrijević, Mirjana AU - Pilipović, Ivan AU - Stanojević, Stanislava AU - Mitić, Katarina AU - Radojević, Katarina AU - Pešić, Vesna AU - Leposavić, Gordana PY - 2009 UR - https://farfar.pharmacy.bg.ac.rs/handle/123456789/1278 AB - Using both immunocytochemical and flow cytometric analyses of rat peritoneal exudate cells constitutive expression of tyrosine hydroxylase and both beta(2)- and alpha(1)-adrenoceptors on macrophages was revealed. Furthermore, according to the characteristic assemblage of tyrosine hydroxylase and adrenoceptor subtype expression different macrophage subsets were identified. In vitro treatment of macrophages with the nonselective alpha,beta-adrenoceptor agonist arterenol and/or the beta-adrenoceptor antagonist propranolol indicated that beta-adrenoceptors potentiated nitric oxide (NO) production and suggested alpha-adrenoceptor-mediated suppression of hydrogen peroxide (H2O2) production. An increase in H2O2 production in the presence of the alpha(1)-adrenoceptor antagonist ebrantil provided support for this. Chronic propranolol treatment in vivo led to increased NO and H2O2 production by peritoneal macrophages. Furthermore, this treatment resulted in opposing effects on the expression Of beta(2)- and alpha(1)-adrenoceptors on peritoneal macrophages (a stimulatory effect on beta(2)-adrenoceptors and a suppressive effect on alpha(1)-adrenoceptors). In conclusion, a subset of resident peritoneal macrophages synthesizes catecholamines, which may exert differential effects on H2O2 and NO production via distinct adrenoceptors. Finally, chronic propranolol treatment affected adrenoceptor expression on peritoneal macrophages and altered their capacity to generate NO and H2O2. PB - Elsevier Science BV, Amsterdam T2 - Journal of Neuroimmunology T1 - Chronic propranolol treatment affects expression of adrenoceptors on peritoneal macrophages and their ability to produce hydrogen peroxide and nitric oxide VL - 211 IS - 1-2 SP - 56 EP - 65 DO - 10.1016/j.jneuroim.2009.03.014 ER -
@article{ author = "Dimitrijević, Mirjana and Pilipović, Ivan and Stanojević, Stanislava and Mitić, Katarina and Radojević, Katarina and Pešić, Vesna and Leposavić, Gordana", year = "2009", abstract = "Using both immunocytochemical and flow cytometric analyses of rat peritoneal exudate cells constitutive expression of tyrosine hydroxylase and both beta(2)- and alpha(1)-adrenoceptors on macrophages was revealed. Furthermore, according to the characteristic assemblage of tyrosine hydroxylase and adrenoceptor subtype expression different macrophage subsets were identified. In vitro treatment of macrophages with the nonselective alpha,beta-adrenoceptor agonist arterenol and/or the beta-adrenoceptor antagonist propranolol indicated that beta-adrenoceptors potentiated nitric oxide (NO) production and suggested alpha-adrenoceptor-mediated suppression of hydrogen peroxide (H2O2) production. An increase in H2O2 production in the presence of the alpha(1)-adrenoceptor antagonist ebrantil provided support for this. Chronic propranolol treatment in vivo led to increased NO and H2O2 production by peritoneal macrophages. Furthermore, this treatment resulted in opposing effects on the expression Of beta(2)- and alpha(1)-adrenoceptors on peritoneal macrophages (a stimulatory effect on beta(2)-adrenoceptors and a suppressive effect on alpha(1)-adrenoceptors). In conclusion, a subset of resident peritoneal macrophages synthesizes catecholamines, which may exert differential effects on H2O2 and NO production via distinct adrenoceptors. Finally, chronic propranolol treatment affected adrenoceptor expression on peritoneal macrophages and altered their capacity to generate NO and H2O2.", publisher = "Elsevier Science BV, Amsterdam", journal = "Journal of Neuroimmunology", title = "Chronic propranolol treatment affects expression of adrenoceptors on peritoneal macrophages and their ability to produce hydrogen peroxide and nitric oxide", volume = "211", number = "1-2", pages = "56-65", doi = "10.1016/j.jneuroim.2009.03.014" }
Dimitrijević, M., Pilipović, I., Stanojević, S., Mitić, K., Radojević, K., Pešić, V.,& Leposavić, G.. (2009). Chronic propranolol treatment affects expression of adrenoceptors on peritoneal macrophages and their ability to produce hydrogen peroxide and nitric oxide. in Journal of Neuroimmunology Elsevier Science BV, Amsterdam., 211(1-2), 56-65. https://doi.org/10.1016/j.jneuroim.2009.03.014
Dimitrijević M, Pilipović I, Stanojević S, Mitić K, Radojević K, Pešić V, Leposavić G. Chronic propranolol treatment affects expression of adrenoceptors on peritoneal macrophages and their ability to produce hydrogen peroxide and nitric oxide. in Journal of Neuroimmunology. 2009;211(1-2):56-65. doi:10.1016/j.jneuroim.2009.03.014 .
Dimitrijević, Mirjana, Pilipović, Ivan, Stanojević, Stanislava, Mitić, Katarina, Radojević, Katarina, Pešić, Vesna, Leposavić, Gordana, "Chronic propranolol treatment affects expression of adrenoceptors on peritoneal macrophages and their ability to produce hydrogen peroxide and nitric oxide" in Journal of Neuroimmunology, 211, no. 1-2 (2009):56-65, https://doi.org/10.1016/j.jneuroim.2009.03.014 . .