Key result
Cardiac overexpression of the β1-adrenoceptor in young, nonfailing mice resulted in largely preserved circadian and short-term regulation of blood pressure and heart rate compared to wildtype mice.
Why the study?
Does elevated cardiac sympathetic activity (via beta1-adrenoceptor overexpression) alter circadian and short-term variability in blood pressure and heart rate in nonfailing mice?
Population
8 to 9-week-old wildtype and transgenic mice with cardiac overexpression of the beta1-adrenoceptor prior to…
Comparison
Propranolol (500mg/L in drinking water) vs Baseline conditions and wildtype controls
Design
Preclinical
Follow-up
24 hours (continuous monitoring)
Authors
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Sympathetic overactivity alone may not explain lost BP/HR variability in human HF; leaves open mechanisms and requires human validation.
Does elevated cardiac sympathetic activity (via beta1-adrenoceptor overexpression) alter circadian and short-term variability in blood pressure and heart rate in nonfailing mice?
Circadian and short-term regulation of blood pressure and heart rate are largely preserved in young, nonfailing beta1-transgenic mice, suggesting that the loss of variability in human heart failure is not solely due to sympathetic overactivity.
Witte et al. (2004) studied Cardiac overexpression of the β1-adrenoceptor. Cardiac overexpression of the β1-adrenoceptor vs. Wildtype mice was evaluated on Circadian and short-term regulation of blood pressure and heart rate. Cardiac overexpression of the β1-adrenoceptor in young, nonfailing mice resulted in largely preserved circadian and short-term regulation of blood pressure and heart rate compared to wildtype mice.
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