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Disruption of cardiovascular circadian rhythms in mice post myocardial infarction: relationship with central angiotensin II receptor expression.

Mousa TM, Schiller AM, Zucker IH - Physiol Rep (2014)

Bottom Line: 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 AT1R and gp91(phox) proteins in the brainstem.Losartan reduced AT1R expression in daytime (1.18 ± 0.1 vs. 0.85 ± 0.1; P < 0.05) with a trend toward a reduction in the AT1R 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 AT1 and gp91(phox) suggests a possible role for central oxidative stress as a mediator of circadian cardiovascular parameters in the post-MI state.

View Article: PubMed Central - PubMed

Affiliation: Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, Nebraska.

No MeSH data available.


Related in: MedlinePlus

Hemodynamic and spontaneous baroreflex sensitivity for both sham and MI mice over time, taken during the daytime (open squares) and nighttime (closed squares). MAP = mean arterial pressure; HR = heart rate; BRS = baroreflex sensitivity. Numbers in parentheses are the n per group.
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fig01: Hemodynamic and spontaneous baroreflex sensitivity for both sham and MI mice over time, taken during the daytime (open squares) and nighttime (closed squares). MAP = mean arterial pressure; HR = heart rate; BRS = baroreflex sensitivity. Numbers in parentheses are the n per group.

Mentions: Figure 1 shows the time course for changes in MAP; panel A, HR; panel B, and BRS; panel C in sham animals (left panels) and in animals post‐MI (right panels) during both nighttime and daytime periods. The sham data were similar at each time period, suggesting that the circadian variability was stable over time and that any difference in MI animals was not the result of time‐dependent changes, but the result of changes taking place after MI. Sham animals exhibited day–night variability for MAP, HR, and BRS. Post‐MI mice exhibited differences between the day–night values for MAP at 2 and 4 weeks and HR at 2 weeks. This difference was lost by 8 weeks post‐MI. Therefore, from 8 to 12 weeks post‐MI, there were no dips in MAP during the daytime. This was associated with a significant drop in EF and increases in the lung weights. In MI mice, the HR increased over time suggesting sympatho‐excitation as cardiac function deteriorates. Interestingly, the day–night difference in HR was still preserved 2 weeks post‐MI. This was lost by 4 weeks (panel B). Panel C illustrates mean data for BRS which was depressed in mice as early as 2 weeks post‐MI even though cardiac function was well preserved at this time point. Moreover, the day–night variability was also lost at 2 weeks post‐MI. There was a further and significant fall in BRS at 4 weeks and for the remainder of the 16 weeks. Note the differences in the scale between sham and MI mice in panel C.


Disruption of cardiovascular circadian rhythms in mice post myocardial infarction: relationship with central angiotensin II receptor expression.

Mousa TM, Schiller AM, Zucker IH - Physiol Rep (2014)

Hemodynamic and spontaneous baroreflex sensitivity for both sham and MI mice over time, taken during the daytime (open squares) and nighttime (closed squares). MAP = mean arterial pressure; HR = heart rate; BRS = baroreflex sensitivity. Numbers in parentheses are the n per group.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4255816&req=5

fig01: Hemodynamic and spontaneous baroreflex sensitivity for both sham and MI mice over time, taken during the daytime (open squares) and nighttime (closed squares). MAP = mean arterial pressure; HR = heart rate; BRS = baroreflex sensitivity. Numbers in parentheses are the n per group.
Mentions: Figure 1 shows the time course for changes in MAP; panel A, HR; panel B, and BRS; panel C in sham animals (left panels) and in animals post‐MI (right panels) during both nighttime and daytime periods. The sham data were similar at each time period, suggesting that the circadian variability was stable over time and that any difference in MI animals was not the result of time‐dependent changes, but the result of changes taking place after MI. Sham animals exhibited day–night variability for MAP, HR, and BRS. Post‐MI mice exhibited differences between the day–night values for MAP at 2 and 4 weeks and HR at 2 weeks. This difference was lost by 8 weeks post‐MI. Therefore, from 8 to 12 weeks post‐MI, there were no dips in MAP during the daytime. This was associated with a significant drop in EF and increases in the lung weights. In MI mice, the HR increased over time suggesting sympatho‐excitation as cardiac function deteriorates. Interestingly, the day–night difference in HR was still preserved 2 weeks post‐MI. This was lost by 4 weeks (panel B). Panel C illustrates mean data for BRS which was depressed in mice as early as 2 weeks post‐MI even though cardiac function was well preserved at this time point. Moreover, the day–night variability was also lost at 2 weeks post‐MI. There was a further and significant fall in BRS at 4 weeks and for the remainder of the 16 weeks. Note the differences in the scale between sham and MI mice in panel C.

Bottom Line: 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 AT1R and gp91(phox) proteins in the brainstem.Losartan reduced AT1R expression in daytime (1.18 ± 0.1 vs. 0.85 ± 0.1; P < 0.05) with a trend toward a reduction in the AT1R 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 AT1 and gp91(phox) suggests a possible role for central oxidative stress as a mediator of circadian cardiovascular parameters in the post-MI state.

View Article: PubMed Central - PubMed

Affiliation: Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, Nebraska.

No MeSH data available.


Related in: MedlinePlus