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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

Day–night comparisons of AT1R protein and mRNA expression in sham and MI mice at 8 weeks. There was a clear increase in brainstem AT1 protein during the nighttime hours in the sham group. MI mice showed an increase in AT1 protein in both daytime and nighttime periods. Losartan treatment lowered daytime expression in MI mice, but had little effect on the nighttime expression. Numbers in parentheses are the n per group.
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fig04: Day–night comparisons of AT1R protein and mRNA expression in sham and MI mice at 8 weeks. There was a clear increase in brainstem AT1 protein during the nighttime hours in the sham group. MI mice showed an increase in AT1 protein in both daytime and nighttime periods. Losartan treatment lowered daytime expression in MI mice, but had little effect on the nighttime expression. Numbers in parentheses are the n per group.

Mentions: We then asked the question whether changes in central AT1Rs and gp91phox could be mediating hemodynamic changes (i.e., MAP, HR, and BRS). In Fig. 4, a day–night pattern of AT1R protein expression was seen in sham animals 8 weeks following surgery. This variation was lost in the MI mice at the same time period. However, losartan infusion for 5 days failed to restore cardiac circadian rhythm, but did restore AT1R protein expression levels. Interestingly, losartan did not have an effect on levels of AT1R mRNA (Fig. 4). This suggests that normalization of the protein and also mRNA of the AT1R could be required to restore circadian rhythm.


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)

Day–night comparisons of AT1R protein and mRNA expression in sham and MI mice at 8 weeks. There was a clear increase in brainstem AT1 protein during the nighttime hours in the sham group. MI mice showed an increase in AT1 protein in both daytime and nighttime periods. Losartan treatment lowered daytime expression in MI mice, but had little effect on the nighttime expression. 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

fig04: Day–night comparisons of AT1R protein and mRNA expression in sham and MI mice at 8 weeks. There was a clear increase in brainstem AT1 protein during the nighttime hours in the sham group. MI mice showed an increase in AT1 protein in both daytime and nighttime periods. Losartan treatment lowered daytime expression in MI mice, but had little effect on the nighttime expression. Numbers in parentheses are the n per group.
Mentions: We then asked the question whether changes in central AT1Rs and gp91phox could be mediating hemodynamic changes (i.e., MAP, HR, and BRS). In Fig. 4, a day–night pattern of AT1R protein expression was seen in sham animals 8 weeks following surgery. This variation was lost in the MI mice at the same time period. However, losartan infusion for 5 days failed to restore cardiac circadian rhythm, but did restore AT1R protein expression levels. Interestingly, losartan did not have an effect on levels of AT1R mRNA (Fig. 4). This suggests that normalization of the protein and also mRNA of the AT1R could be required to restore circadian rhythm.

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