Open AccessDisruption of cardiovascular circadian rhythms in mice post myocardial infarction: relationship with central angiotensin II receptor expression
Author(s) -
Mousa Tarek M.,
Schiller Alicia M.,
Zucker Irving H.
Publication year - 2014
Publication title -
physiological reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.918
H-Index - 39
ISSN - 2051-817X
DOI - 10.14814/phy2.12210
Subject(s) - circadian rhythm , medicine , endocrinology , angiotensin ii , baroreflex , losartan , angiotensin ii receptor type 1 , downregulation and upregulation , myocardial infarction , cardiology , heart rate , blood pressure , biology , biochemistry , gene
Angiotensin II (Ang II) is well known to participate in the abnormal autonomic cardiovascular control that occurs during the development of chronic heart failure ( CHF ). Disrupted cardiovascular circadian rhythm in CHF is also well accepted; however, the mechanisms underlying and the role of central Ang II type 1 receptors ( AT 1 R ) and oxidative stress in mediating such changes are not clear. In a post myocardial infarction ( MI ) CHF mouse model we investigated the circadian rhythm for mean arterial pressure ( MAP ), heart rate ( HR ), and baroreflex sensitivity ( BRS ) following MI . The cardiovascular parameters represent the middle 6‐h averages during daytime (6:00–18:00) and nighttime (18:00–6:00). HR increased with the severity of CHF reaching its maximum by 12 weeks post‐ MI ; loss of circadian HR and BRS rhythms were observed as early as 4 weeks post‐ MI in conjunction with a significant blunting of the BRS and an upregulation in the AT 1 R and gp91 phox proteins in the brainstem. Loss of MAP circadian rhythm was observed 8 weeks post‐ MI . Circadian AT 1 R expression was demonstrated in sham animals but was lost 8 weeks following MI . Losartan reduced AT 1 R expression in daytime (1.18 ± 0.1 vs. 0.85 ± 0.1; P < 0.05) with a trend toward a reduction in the AT 1 R mRNA expression in the nighttime (1.2 ± 0.1 vs. 1.0 ± 0.1; P > 0.05) but failed to restore circadian variability. The disruption of circadian rhythm for HR , MAP and BRS along with the upregulation of AT 1 and gp91 phox suggests a possible role for central oxidative stress as a mediator of circadian cardiovascular parameters in the post‐ MI state.