title: The cardiac expression of Mas receptor is responsive to different physiological and pathological stimuli.
abstract: The Mas protooncogene encodes a G protein-coupled receptor that has been described as a functional receptor for the cardioprotective fragment of the renin-angiotensin system (RAS), Angiotensin (Ang)-(1-7). The aim of this current study was to evaluate the responsiveness of Mas expression in hearts during different physiological and pathological conditions in rats. Physical training was considered a physiological condition, while isoproterenol-induced hypertrophy, myocardial infarction and DOCA-salt model of hypertension were used as pathological models of heart injury. The expression of Mas was analyzed by western blotting. Although swim-trained rats presented significant cardiac hypertrophy, our physical training protocol was unable to induce changes in the expression of Mas. On the other hand, cardiac hypertrophy and damage elicited by isoproterenol treatment led to a reduction in Mas expression. Myocardial infarction also significantly decreased the expression of Mas after 21 days of myocardial ischemia. Additionally, Mas expression levels were increased in hearts of DOCA-salt rats. Our present data indicate that Mas expression is responsive to different pathological stimuli, thereby suggesting that Mas receptor is involved in the homeostasis of the heart, as well as in the establishment and progression of cardiac diseases.
authors.affiliation: Department of Physiology and Biophysics, Federal University of Minas Gerais, Belo Horizonte, MG, Brazil.
authors.forename: Marco Fabricio
authors.initials: MF
authors.lastname: Dias-Peixoto
authors.forename: Anderson J
authors.initials: AJ
authors.lastname: Ferreira
authors.forename: Pedro W M
authors.initials: PW
authors.lastname: Almeida
authors.forename: Vinícius B A
authors.initials: VB
authors.lastname: Braga
authors.forename: Danielle C O
authors.initials: DC
authors.lastname: Coutinho
authors.forename: Dirceu S
authors.initials: DS
authors.lastname: Melo
authors.forename: Ary
authors.initials: A
authors.lastname: Gomes Filho
authors.forename: Marcos B
authors.initials: MB
authors.lastname: Melo
authors.forename: Leonardo
authors.initials: L
authors.lastname: Greco
authors.forename: Maria José
authors.initials: MJ
authors.lastname: Campagnole-Santos
authors.forename: Ricardo F
authors.initials: RF
authors.lastname: Lima
authors.forename: Robson A S
authors.initials: RA
authors.lastname: Santos
authors.forename: Silvia
authors.initials: S
authors.lastname: Guatimosim
mesh_terms: D000803:Angiotensin I / Q000378:metabolism; D000818:Animals; D006332:Cardiomegaly / Q000139:chemically induced / Q000378:metabolism*; D003900:Desoxycorticosterone; D006973:Hypertension / Q000378:metabolism*; D007545:Isoproterenol; D008297:Male; D009043:Motor Activity; D009203:Myocardial Infarction / Q000378:metabolism*; D009206:Myocardium / Q000378:metabolism*; D010446:Peptide Fragments / Q000378:metabolism; D010805:Physical Conditioning, Animal; D000090063:Proto-Oncogene Mas; D011518:Proto-Oncogene Proteins / Q000096:biosynthesis / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D017208:Rats, Wistar; D043562:Receptors, G-Protein-Coupled / Q000096:biosynthesis / Q000378:metabolism*
chemical_list: D010446:Peptide Fragments; D000090063:Proto-Oncogene Mas; D011518:Proto-Oncogene Proteins; D043562:Receptors, G-Protein-Coupled; D003900:Desoxycorticosterone; D000803:Angiotensin I; C118790:angiotensin I (1-7); D007545:Isoproterenol