title: Cardiovascular role of angiotensin type1A receptors in the nucleus of the solitary tract of mice.
abstract: OBJECTIVE
  The nucleus of the solitary tract (NTS) is important for cardiovascular regulation and contains angiotensin type 1A (AT1A) receptors. To assess its function, we examined the effect of expressing in AT1A receptors in the NTS of mice lacking these receptors.
  
  
  RESULTS
  Bilateral microinjections of lentivirus expressing AT1A receptors (AT1Av mice, n = 6) or green fluorescent protein (GFPv, n = 8, control) under the control of the PRSx8 promotor were made into the NTS of AT1A receptors null mice (AT1A(-/-)). Telemetry devices recorded blood pressure (BP), heart rate (HR), and locomotor activity. Expression of AT1A receptors in the NTS increased BP by 11.2 ± 4 mmHg (P < 0.05) at 2 and 3 weeks, whereas GFPv mice remained at pre-injection BP. Ganglion blockade reduced BP to similar levels pre- and post-transfection in GFPv and AT1Av mice. Greater pressor responses to cage-switch stress were observed following AT1A receptors expression (+18 ± 2 mmHg pre- to +24 ± 2 mmHg post-virus, P < 0.05) with similar stress-induced pressor responses pre- and post-virus in GFPv mice. Pressor responses to restraint stress pre- and post-virus were similar in AT1Av but were 20% less post-GFPv (P < 0.001). The lack of attenuation in BP to restraint was associated with four-fold greater Fos-expression in AT1A receptors mice. AT1A receptors expression in the NTS did not alter baroreflex gain differently between groups.
  
  
  CONCLUSIONS
  The results suggest that transfection of AT1A receptors on neurons in the NTS elevates BP independent of the SNS and pressor responses to aversive stimuli are associated with greater Fos-expression in forebrain regions. This study suggests a novel mechanism by which the NTS may modulate MAP in the long-term via AT1A receptors.
authors.affiliation: Neuropharmacology Laboratory, Baker IDI Heart and Diabetes Research Institute, Melbourne, Victoria 8008, Australia.
authors.forename: Beza
authors.initials: B
authors.lastname: Abegaz
authors.forename: Pamela J
authors.initials: PJ
authors.lastname: Davern
authors.forename: Kristy L
authors.initials: KL
authors.lastname: Jackson
authors.forename: Thu-Phuc
authors.initials: TP
authors.lastname: Nguyen-Huu
authors.forename: Jaspreet K
authors.initials: JK
authors.lastname: Bassi
authors.forename: Angela
authors.initials: A
authors.lastname: Connelly
authors.forename: Yan-Ting
authors.initials: YT
authors.lastname: Choong
authors.forename: Andrew M
authors.initials: AM
authors.lastname: Allen
authors.forename: Geoffrey A
authors.initials: GA
authors.lastname: Head
mesh_terms: D000818:Animals; D062186:Arterial Pressure / Q000502:physiology*; D001345:Autoradiography; D017704:Baroreflex; D006339:Heart Rate / Q000502:physiology*; D007150:Immunohistochemistry; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009043:Motor Activity; D010425:Pentolinium Tartrate / Q000494:pharmacology; D016760:Proto-Oncogene Proteins c-fos / Q000032:analysis; D044140:Receptor, Angiotensin, Type 1 / Q000502:physiology*; D017552:Solitary Nucleus / Q000502:physiology*; D013315:Stress, Psychological / Q000503:physiopathology
chemical_list: D016760:Proto-Oncogene Proteins c-fos; D044140:Receptor, Angiotensin, Type 1; D010425:Pentolinium Tartrate
keywords: Angiotensin type 1A receptor; Baroreflex gain; Cardiovascular stress response; Nucleus of the solitary tract