title: Increased vascular sympathetic modulation in mice with Mas receptor deficiency.
abstract: BACKGROUND
  The angiotensin-converting enzyme 2 (ACE2)/angiotensin (Ang)-(1-7)/Mas axis could modulate the heart rate (HR) and blood pressure variabilities (BPV) which are important predictors of cardiovascular risk and provide information about the autonomic modulation of the cardiovascular system. Therefore we investigated the effect of Mas deficiency on autonomic modulation in wild type and Mas-knockout (KO) mice.
  
  
  METHODS
  Blood pressure was recorded at high sample rate (4000 Hz). Stationary sequences of 200-250 beats were randomly chosen. Frequency domain analysis of HR and BPV was performed with an autoregressive algorithm on the pulse interval sequences and on respective systolic sequences.
  
  
  RESULTS
  The KO group presented an increase of systolic arterial pressure (SAP; 127.26±11.20 vs 135.07±6.98 mmHg), BPV (3.54±1.54 vs 5.87±2.12 mmHg(2)), and low-frequency component of systolic BPV (0.12±0.11 vs 0.47±0.34 mmHg(2)).
  
  
  CONCLUSIONS
  The deletion of Mas receptor is associated with an increase of SAP and with an increased BPV, indicating alterations in autonomic control. Increase of sympathetic vascular modulation in absence of Mas evidences the important role of Ang-(1-7)/Mas on cardiovascular regulation. Moreover, the absence of significant changes in HR and HRV can indicate an adaptation of autonomic cardiac balance. Our results suggest that the Ang-(1-7)/Mas axis seems more important in autonomic modulation of arterial pressure than HR.
authors.affiliation: Universidade Federal de São Paulo, São Paulo, Brazil Instituto de Cardiologia-Fundação Universitária de Cardiologia, Porto Alegre, RS, Brazil.
authors.forename: Karina
authors.initials: K
authors.lastname: Rabello Casali
authors.affiliation: Instituto de Cardiologia-Fundação Universitária de Cardiologia, Porto Alegre, RS, Brazil.
authors.forename: Daniela
authors.initials: D
authors.lastname: Ravizzoni Dartora
authors.affiliation: Max-Delbruck Center for Molecular Medicine, Berlin, Germany.
authors.forename: Marina
authors.initials: M
authors.lastname: Moura
authors.affiliation: CHU Sainte Justine Research, Montreal, Canada.
authors.forename: Mariane
authors.initials: M
authors.lastname: Bertagnolli
authors.affiliation: Max-Delbruck Center for Molecular Medicine, Berlin, Germany.
authors.forename: Michael
authors.initials: M
authors.lastname: Bader
authors.affiliation: Max-Delbruck Center for Molecular Medicine, Berlin, Germany.
authors.forename: Andrea
authors.initials: A
authors.lastname: Haibara
authors.affiliation: Max-Delbruck Center for Molecular Medicine, Berlin, Germany.
authors.forename: Natalia
authors.initials: N
authors.lastname: Alenina
authors.affiliation: Instituto de Cardiologia-Fundação Universitária de Cardiologia, Porto Alegre, RS, Brazil Instituto do Coração (InCor), São Paulo, Brazil.
authors.forename: Maria Claudia
authors.initials: MC
authors.lastname: Irigoyen
authors.affiliation: Instituto de Cardiologia-Fundação Universitária de Cardiologia, Porto Alegre, RS, Brazil National Institute of Science and Technology in Nanobiopharmaceutics, Belo Horizonte, Brazil robsonsant@gmail.com.
authors.forename: Robson A
authors.initials: RA
authors.lastname: Santos
mesh_terms: D000818:Animals; D001808:Blood Vessels / Q000378:metabolism*; D006439:Hemodynamics; D008297:Male; D018345:Mice, Knockout; D000090063:Proto-Oncogene Mas; D011518:Proto-Oncogene Proteins / Q000172:deficiency* / Q000378:metabolism; D043562:Receptors, G-Protein-Coupled / Q000172:deficiency* / Q000378:metabolism; D013564:Sympathetic Nervous System / Q000378:metabolism*; D013599:Systole
chemical_list: D000090063:Proto-Oncogene Mas; D011518:Proto-Oncogene Proteins; D043562:Receptors, G-Protein-Coupled
keywords: Mas receptor; Renin–angiotensin system; angiotensin-(1–7); autonomic modulation; blood pressure variability; heart rate variability