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Chronic propranolol treatment affects expression of adrenoceptors on peritoneal macrophages and their ability to produce hydrogen peroxide and nitric oxide

Само за регистроване кориснике
2009
Аутори
Dimitrijević, Mirjana
Pilipović, Ivan
Stanojević, Stanislava
Mitić, Katarina
Radojević, Katarina
Pešić, Vesna
Leposavić, Gordana
Чланак у часопису (Објављена верзија)
Метаподаци
Приказ свих података о документу
Апстракт
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. (C) 2009 Elsevier B.V. All rights reserved.

Кључне речи:
alpha-adrenoceptor / beta-adrenoceptor / Catecholamines / Macrophages / Rat
Извор:
Journal of Neuroimmunology, 2009, 211, 1-2, 56-65
Издавач:
  • Elsevier, Amsterdam
Финансирање / пројекти:
  • Неуроендокрина модулација имунског одговора: улога симпато-адреномедуларног система (RS-145049)

DOI: 10.1016/j.jneuroim.2009.03.014

ISSN: 0165-5728

PubMed: 19398131

WoS: 000268035000006

Scopus: 2-s2.0-67349256113
[ Google Scholar ]
13
13
URI
http://intor.torlakinstitut.com/handle/123456789/273
Колекције
  • Radovi istraživača / Researchers’ publications
Институција/група
Torlak
TY  - 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  - http://intor.torlakinstitut.com/handle/123456789/273
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. (C) 2009 Elsevier B.V. All rights reserved.
PB  - Elsevier, 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
EP  - 65
IS  - 1-2
SP  - 56
VL  - 211
DO  - 10.1016/j.jneuroim.2009.03.014
UR  - conv_238
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. (C) 2009 Elsevier B.V. All rights reserved.",
publisher = "Elsevier, 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",
pages = "65-56",
number = "1-2",
volume = "211",
doi = "10.1016/j.jneuroim.2009.03.014",
url = "conv_238"
}
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, Amsterdam., 211(1-2), 56-65.
https://doi.org/10.1016/j.jneuroim.2009.03.014
conv_238
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
conv_238 .
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 .,
conv_238 .

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