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Screening genetico nella FA e nei disturbi di conduzione : dati della letteratura e in quali pazienti
No full textScreening genetico nella FA e nei disturbi di conduzione : dati della letteratura e in quali pazienti
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Pharmacological characterization of fast inward sodium currents in rabbit currents in rabbit sino-atrial node and atrial myocytes
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A TTX-sensitive inward sodium current contributes to spontaneous activity in newborn rabbit sino-atrial node cells
No full text1. Subcellularly localized Ca2+ signals have been proposed to represent elementary events of cardiac Ca2+ signalling (Ca2+ sparks), whereby an individual sarcolemmal L-type Ca2+ channel locally controls opening of a single (or a few) Ca2+ release channels in the sarcoplasmic reticulum (SR). 2. To investigate directly the elementary nature of this Ca(2+)-induced Ca2+ release mechanism we used flash photolysis of caged Ca2+ while simultaneously measuring the intracellular Ca2+ concentration ([Ca2+]i) with a laser-scanning confocal microscope. 3. Power spectral analysis of the confocal images performed in the spatial domain revealed that only Ca2+ signalling events involving the L-type Ca2+ channel pathway gave rise to Ca2+ sparks. In contrast, SR Ca2+ release triggered by photolytic [Ca2+]i jumps resulted in Ca2+ transients that were always spatially homogeneous. 4. From these findings we conclude that the fundamental event of Ca2+ signalling in cardiac muscle may be smaller in size or amplitude than a Ca2+ spark. 5. We term this event a 'Ca2+ quark' possibly resulting from gating of a single SR Ca2+ release channel. It is proposed that concerted activation of several 'Ca2+ quarks' may be required for a Ca2+ spark. The 'Ca2+ quark' could also be the fundamental event in other cell types implementing a hierarchical Ca2+ signalling concept
The newborn rabbit sino-atrial node expresses an inward sodium current with novel pharmacological characteristics
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Na+ current contribution to the diastolic depolarization in newborn rabbit SA node cells
No full textIsolated newborn, but not adult, rabbit sinoatrial node (SAN) cells exhibit spontaneous activity that (unlike adult) are highly sensitive to the Na+ current (I-Na) blocker TTX. To investigate this TTX action on automaticity, cells were voltage clamped with ramp depolarizations mimicking the pacemaker phase of spontaneous cells (-60 to -20 mV, 35 mV/s). Ramps elicited a TTX-sensitive current in newborn (peak density 0.89 +/- 0.14 pA/pF, n = 24) but not adult (n = 5) cells. When depolarizing ramps were preceded by steplike depolarizations to mimic action potentials, ramp current decreased 54.6 +/- 8.0% (n = 3) but was not abolished. Additional experiments demonstrated that ramp current amplitude depended on the slope of the ramp and that TTX did not alter steady-state holding current at pacemaker potentials. This excluded a steady-state Na+ window component and suggested a kinetic basis, which was investigated by measuring TTX-sensitive I-Na during long step depolarizations. I-Na exhibited a slow but complete inactivation time course at pacemaker voltages (tau = 33.9 +/- 3.9 ms at -50 mV), consistent with the rate-dependent ramp data. The data indicate that owing to slow inactivation of I-Na at diastolic potentials, a small TTX-sensitive current flows during the diastolic depolarization in neonatal pacemaker myocytes
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