title: Participation of AT1 and Mas receptors in the modulation of inflammatory pain.
abstract: We investigated the mechanisms underlying the endogenous control of nociception at the peripheral level during inflammation. We hypothesized that angiotensin receptors could modulate pain at the peripheral level via endogenous processes because angiotensin receptors are present in peripheral nerve terminals. We evaluated the role of the angiotensin receptors system (RAS) in the modulation of inflammatory and neuropathic pain states. Mas receptor KO mice exhibited major inflammatory pain compared to wild-type mice. Similar results were observed when rats were injected with the Mas receptor antagonist A779 or the AT1 receptor antagonist, losartan after inflammatory stimulation by carrageenan. However, these antagonists were not effective in animals with neuropathic-induced pain (e.g., sciatic nerve constriction). Therefore, RAS seems to play an important role in inflammatory but not neuropathic pain.
authors.affiliation: Department of Pharmacology, Institute of Biological Sciences, UFMG, 31270901 Belo Horizonte, Brazil.
authors.forename: Aline C O
authors.initials: AC
authors.lastname: Costa
authors.affiliation: Department of Pharmacology, Institute of Biological Sciences, UFMG, 31270901 Belo Horizonte, Brazil.
authors.forename: Thiago R L
authors.initials: TR
authors.lastname: Romero
authors.affiliation: Department of Pharmacology, Institute of Biological Sciences, UFMG, 31270901 Belo Horizonte, Brazil.
authors.forename: Daniela F
authors.initials: DF
authors.lastname: Pacheco
authors.affiliation: Department of Pharmacology, Institute of Biological Sciences, UFMG, 31270901 Belo Horizonte, Brazil.
authors.forename: Andrea C
authors.initials: AC
authors.lastname: Perez
authors.affiliation: Department of Pharmacology, Institute of Biological Sciences, UFMG, 31270901 Belo Horizonte, Brazil.
authors.forename: Atila
authors.initials: A
authors.lastname: Savernini
authors.affiliation: Department of Physiology, Institute of Biological Sciences, UFMG, 31270901 Belo Horizonte, Brazil.
authors.forename: Robson R A
authors.initials: RR
authors.lastname: Santos
authors.affiliation: Department of Pharmacology, Institute of Biological Sciences, UFMG, 31270901 Belo Horizonte, Brazil. Electronic address: dimitri@icb.ufmg.br.
authors.forename: Igor D G
authors.initials: ID
authors.lastname: Duarte
mesh_terms: D000804:Angiotensin II / Q000031:analogs & derivatives* / Q000494:pharmacology; D047228:Angiotensin II Type 1 Receptor Blockers / Q000494:pharmacology*; D000818:Animals; D007249:Inflammation / Q000188:drug therapy / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D019808:Losartan / Q000494:pharmacology*; D008297:Male; D051379:Mice; D018345:Mice, Knockout; D010146:Pain / Q000188:drug therapy / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D010446:Peptide Fragments / Q000494:pharmacology*; D000090063:Proto-Oncogene Mas; D011518:Proto-Oncogene Proteins / Q000037:antagonists & inhibitors* / Q000235:genetics / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D044140:Receptor, Angiotensin, Type 1 / Q000235:genetics / Q000378:metabolism*; D043562:Receptors, G-Protein-Coupled / Q000037:antagonists & inhibitors* / Q000235:genetics / Q000378:metabolism*
chemical_list: C092006:7-Ala-angiotensin (1-7); D047228:Angiotensin II Type 1 Receptor Blockers; D010446:Peptide Fragments; D000090063:Proto-Oncogene Mas; D011518:Proto-Oncogene Proteins; D044140:Receptor, Angiotensin, Type 1; D043562:Receptors, G-Protein-Coupled; D000804:Angiotensin II; D019808:Losartan
keywords: Angiotensin; Carrageenan hyperalgesia; Inflammation; Peripheral pain control