Key result
Local Ca2+ releases impart a nonlinear, exponentially rising phase to the late diastolic depolarization that controls the spontaneous firing rate of rabbit sinoatrial nodal cells.
Why the study?
How do local subsarcolemmal ryanodine receptor-mediated Ca2+ releases (LCRs) impact the late diastolic depolarization to control spontaneous firing rate in rabbit sinoatrial nodal cells?
Population
Rabbit sinoatrial nodal pacemaker cells (SANCs)
Design
Preclinical
Authors
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LCR-NCX coupling may modulate SANC rate; leaves open in vivo validation or therapeutic targeting.
How do local subsarcolemmal ryanodine receptor-mediated Ca2+ releases (LCRs) impact the late diastolic depolarization to control spontaneous firing rate in rabbit sinoatrial nodal cells?
Beat-to-beat membrane potential fluctuations during late diastolic depolarization reflect underlying LCR/INCX events that form a nonlinear component controlling the chronotropic state of sinoatrial nodal cells.
Bogdanov et al. (2006) studied Sinoatrial nodal pacemaker cell function. Maneuvers altering LCR timing or amplitude (ryanodine, BAPTA, nifedipine, isoproterenol) was evaluated on Membrane potential (Vm) fluctuations and spontaneous beating rate. Local Ca2+ releases impart a nonlinear, exponentially rising phase to the late diastolic depolarization that controls the spontaneous firing rate of rabbit sinoatrial nodal cells.
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