Key result
In swine with tachycardia-induced heart failure, basal peak outward NCX current was increased almost 5-fold, but responsiveness to beta-adrenergic stimulation was significantly reduced (P<0.01).
Population
Swine myocytes with and without tachycardia-induced heart failure
Comparison
Beta-adrenergic receptor stimulation vs Control swine myocytes and basal state
Design
Preclinical
Authors
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Altered NCX regulation in swine HF is hypothesis-generating; leaves open whether targeting NCX phosphorylation improves human outcomes.
p-value: p=<0.01
In a swine model of heart failure, NCX expression and basal activity are increased due to hyperphosphorylation, which blunts its responsiveness to beta-adrenergic stimulation.
Wei et al. (2003) studied Tachycardia-induced heart failure. Tachycardia-induced heart failure vs. Control swine was evaluated on NCX expression level and functional activity (p=<0.01). In swine with tachycardia-induced heart failure, basal peak outward NCX current was increased almost 5-fold, but responsiveness to beta-adrenergic stimulation was significantly reduced (P<0.01).
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