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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

gp91phox protein and mRNA expression in the brainstem of mice at various time periods post‐MI compared to a group of sham‐operated mice. Samples acquired during the daytime period. For sham protein n = 5. For sham mRNA, n = 9. For post‐MI time points n = 5 per time period.
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fig03: gp91phox protein and mRNA expression in the brainstem of mice at various time periods post‐MI compared to a group of sham‐operated mice. Samples acquired during the daytime period. For sham protein n = 5. For sham mRNA, n = 9. For post‐MI time points n = 5 per time period.

Mentions: Because central AT1Rs have been shown to play a role in the sympatho‐excitatory process (Reid 1992; Zucker et al. 2001, 2009), we determined if a correlation of these hemodynamic changes existed with AT1R protein and/or oxidative stress in the central nervous system, specifically in the brain stem. Figure 2 shows AT1R protein and mRNA expression at different time intervals following MI or sham surgery. The left panel shows representative western blots and mean data from each time period and from sham mice. Note we do not show 2‐week molecular data. AT1R mRNA measured by qRT‐PCR (right panel) followed a similar pattern to that of the protein expression. There was approximately a twofold increase in protein and a threefold increase in mRNA. It would appear that AT1R expression was inversely related to the EF which did not fall until 4 weeks post‐MI. Tissue from the cerebral cortex did not show any changes among groups studied (data not shown). Figure 3 shows the protein and message expression for gp91phox, a marker of oxidative stress, as one of the components of the Ang II‐mediated NADPH oxidase subunits. There was approximately a 0.5‐fold change in gp91phox protein and message.


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)

gp91phox protein and mRNA expression in the brainstem of mice at various time periods post‐MI compared to a group of sham‐operated mice. Samples acquired during the daytime period. For sham protein n = 5. For sham mRNA, n = 9. For post‐MI time points n = 5 per time period.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig03: gp91phox protein and mRNA expression in the brainstem of mice at various time periods post‐MI compared to a group of sham‐operated mice. Samples acquired during the daytime period. For sham protein n = 5. For sham mRNA, n = 9. For post‐MI time points n = 5 per time period.
Mentions: Because central AT1Rs have been shown to play a role in the sympatho‐excitatory process (Reid 1992; Zucker et al. 2001, 2009), we determined if a correlation of these hemodynamic changes existed with AT1R protein and/or oxidative stress in the central nervous system, specifically in the brain stem. Figure 2 shows AT1R protein and mRNA expression at different time intervals following MI or sham surgery. The left panel shows representative western blots and mean data from each time period and from sham mice. Note we do not show 2‐week molecular data. AT1R mRNA measured by qRT‐PCR (right panel) followed a similar pattern to that of the protein expression. There was approximately a twofold increase in protein and a threefold increase in mRNA. It would appear that AT1R expression was inversely related to the EF which did not fall until 4 weeks post‐MI. Tissue from the cerebral cortex did not show any changes among groups studied (data not shown). Figure 3 shows the protein and message expression for gp91phox, a marker of oxidative stress, as one of the components of the Ang II‐mediated NADPH oxidase subunits. There was approximately a 0.5‐fold change in gp91phox protein and message.

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