title: Opposite regulation of brain angiotensin type 1 and type 2 receptors in cold-induced hypertension.
abstract: Rats exposed chronically to mild cold (5 degrees C/41 degrees F) develop hypertension. This cold-induced hypertension (CIH) is an environmentally induced, non-surgical, non-pharmacological and non-genetic model for studying hypertension in rats. The blood renin angiotensin system (RAS) appears to play a role in both initiating and maintaining the high blood pressure in CIH. The goal of the present study was to evaluate the role of brain angiotensin type 1 and type 2 receptors (AT1R and AT2R) in CIH. Sprague-Dawley adult male rats were used. Thirty-six rats were kept in a cold room at 5 degrees C and the other 36 were kept at 24 degrees C as controls. Systolic blood pressure (SBP) was recorded by tail cuff. The SBP was elevated in rats exposed to cold within 1 week (n=12, P>0.05), significantly increased at 3 weeks (P<0.05) and reached a maximum (125%) at 5 weeks (P<0.01). Three subgroups of the cold-treated and the controls were sacrificed at 1, 3 and 5 weeks. Specific brain sections were removed, either for reverse transcription polymerase chain reaction (RT-PCR) to measure mRNA, or for autoradiography to measure receptor binding for AT1R and AT2R. The AT1R mRNA was increased significantly in hypothalamus and brainstem after the first week in cold-treated rats and was maintained throughout the time of exposure to cold (n=6, P<0.01). AT1R binding significantly increased initially in hypothalamus and thereafter in brainstem. The mRNA and the receptor binding for AT2R decreased significantly (P<0.01, n=6) in nucleus of inferior olive and locus coeruleus of brainstem in cold-treated rats after exposure to cold. The experiments show differential regulation of RAS components, AT1R and AT2R, in different brain areas in cold-exposed rats and provide evidence that up-regulated AT1R and down-regulated AT2R in different brain areas are involved in CIH. The opposing directions of expression of AT1R and AT2R suggest that they play counterbalancing roles in brain function.
authors.affiliation: Department of Physiology, Box 100274, College of Medicine, University of Florida, Gainesville, FL 32610, USA.
authors.forename: J F
authors.initials: JF
authors.lastname: Peng
authors.forename: M I
authors.initials: MI
authors.lastname: Phillips
mesh_terms: D000803:Angiotensin I / Q000378:metabolism*; D000804:Angiotensin II / Q000378:metabolism*; D000818:Animals; D001345:Autoradiography; D001921:Brain / Q000378:metabolism*; D003080:Cold Temperature; D006973:Hypertension / Q000209:etiology / Q000378:metabolism*; D008297:Male; D011485:Protein Binding; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D011945:Receptors, Angiotensin / Q000235:genetics / Q000378:metabolism*; D020133:Reverse Transcriptase Polymerase Chain Reaction
chemical_list: D012333:RNA, Messenger; D011945:Receptors, Angiotensin; D000804:Angiotensin II; D000803:Angiotensin I