Key result
Pressure overload-induced cardiac hypertrophy reduced the contractile response to dobutamine (increase in FAC 0.10 vs 0.30 in controls; P<0.01), associated with increased PLB-Thr17 phosphorylation.
Absolute Event Rate: 0.1% vs 0.3%
p-value: p=<0.01
In a feline model of pressure overload, increased basal PLB-Thr17 phosphorylation via CaMKII activation contributes to blunted adrenergic contractile responsiveness in cardiac hypertrophy.
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Suggests mechanism limiting inotrope response in hypertrophy; leaves open CaMKII-PLB targeting for clinical translation.
Mills et al. (2006) studied Pressure overload-induced cardiac hypertrophy (n=15). Pressure overload (aortic constriction) vs. Control was evaluated on Contractile response to adrenergic agonists (increase in fractional area change with dobutamine) (p=<0.01). Pressure overload-induced cardiac hypertrophy reduced the contractile response to dobutamine (increase in FAC 0.10 vs 0.30 in controls; P<0.01), associated with increased PLB-Thr17 phosphorylation.
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