Abstract
A common feature of stress cardiomyopathy is contractile impairment of the left ventricular (LV) apical myocardium, although sympathetic effectors are elevated. We investigated the responsiveness of murine cardiomyocytes (CMs) from different LV regions to beta-2 adrenergic (beta2AR) stimulation. Although, initially positively inotropic, beta2AR may become negatively inotropic via biassed-agonism. The apical myocardium may express more beta2ARs as it’s relatively reliant on inotropic support from circulating adrenaline. High initial beta2AR-cAMP activation may initiate stimulus trafficking to beta2AR-Gi signalling. Contractile response to beta2AR stimulation (1µM Isoprenaline with 300nM CGP20712A) was measured by video microscopy. Whole-cell cAMP production after beta2AR stimulation was measured by FRET-based cAMP sensors. Apical CMs (ApCMs) significantly increased their initial contractility following beta2AR stimulation compared to Basal CMs (BCMs) from rats (ApCM 2.28 fold ±0.12 n=10 vs. BCM 1.32 fold ±0.06 n=8 p
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