Abstract
Progressive, age-associated CaV1.2 hypo-responsivity to β-adrenergic receptor (βAR)-stimulation occurs in both human and animal hearts, reducing inotropic reserve and diminishing their capacity to manage episodes of acute stress. Disruption of this crucial regulatory mechanism lowers the threshold for heart failure, yet the causal links between aging and βAR hypo-responsivity remain unclear. We have previously reported that a pre-synthesized pool of sub-sarcolemmal CaV1.2-containing vesicles/endosomes resides in cardiomyocytes and can be mobilized to the sarcolemma in response to βAR stimulation to tune EC-coupling.
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