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Figure 1 | Cardiovascular Ultrasound

Figure 1

From: Myocardial contractility in the echo lab: molecular, cellular and pathophysiological basis

Figure 1

High frequency-induced upregulation of human cardiac calcium currents in isolated cardiomyocytes. Up regulation of Ca2+ entry through Ca2+ channels by high rates of beating is involved in the frequency-dependent regulation of contractility: for each increasing heart rate the steady state is reached rapidly (within few seconds, on the left : FFR). Beta-adrenergic receptor stimulation produces an important enhancement of the force-frequency relation on myocardial contractility: β-adrenergic stimulation, by means of cyclic adenosine monophosphate, promotes phosphorylation and the opening probability of the Ca2+ channel. The effect of increasing contractility by increasing heart rate ("pure" Bowditch treppe) is intrinsic to myocardium and takes few seconds to occur, while the β-adrenergic amplification of the force-frequency relation takes longer, i.e. 30–40 seconds, the time it takes for β-receptor activation and cAMP synthesis (on the right: FFR + ISO). (Modified from: Piot C, Lemaire S, Albat B, et al. High frequency-induced upregulation of human cardiac calcium currents. Circ 1996; 93:120–8)

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