Role of calcium ions in transient inward currents and aftercontractions induced by strophanthidin in cardiac Purkinje fibres.

Abstract

3. TI was closely associated with a phasic increase in force ('aftercontraction'). Like TI, the aftercontraction was evoked by a preceding action potential or by the break of a strong depolarizing pulse.4. TI and the aftercontraction displayed similar wave forms although peak current preceded peak force by 50-100 msec. Both transients were enhanced by increasing the strength or duration of the preceding depolarization pulse. Both events were slowed as the potential level following the pulse was displaced in the negative direction.5. TI and the aftercontraction could be evoked in the absence of cardiotonic steroids by strongly elevating Ca0.6. Additional experiments were carried out to test the hypothesis that TI reflects an influx of Ca2+ ions. Mn inhibited TI but the development and removal of the inhibition lagged far behind the effects on the slow inward current.7. TI could be suppressed and eventually inverted by varying the membrane potential in the positive direction. The inversion potential averaged -5 mV and was not consistent with a Ca-specific pathway. The aftercontraction was more closely related to the phasic conductance change underlying the current than to the current flow itself.8. The results are consistent with the idea that an oscillatory release of Ca from an intracellular store is the primary event underlying both the aftercontraction and the conductance change which generates TI. Digitalis intoxication or very high Cao may promote such events by elevating intracellular Ca levels.

Suppression of voltage-gated L-type Ca 2+ currents by polyunsaturated fatty acids in adult and neonatal rat ventricular myocytes

“…In this study we examine the role of I Ca,L and sarcoplasmic reticulum (SR) Ca 2ϩ release in the action of PUFAs on cardiac myocytes. We observe clear reductions in I Ca,L and SR Ca 2ϩ release, both important in Ca 2ϩ overload arrhythmias (11)(12)(13)(14)(15). We find that the direct action of PUFAs responsible for the reduced SR Ca 2ϩ release is on I Ca,L .…”

Magnesium levels in plasma and erythrocytes before and after histamine challenge

“…Regarding pharmacological effects, several mechanisms have been proposed to explain the potential beneficial effect of magnesium in asthma. It has been shown to relax airway smooth muscle in vitro [2], probably by the modulation of calcium ion movement within the cell [20] and through transmembrane calcium channels [21,22], as well as to broncho;dilate asthmatic airways in vivo [4,5]. It has been demonstrated that histamine and methacholine PD20 threshold dose is moved to the right when the patients were pretreated with aerolized magnesium sulfate, with this effect considered to be similar than that observed with calcium channel blockers [6,7].…”

The Ca2+ leak paradox and “rogue ryanodine receptors”: SR Ca2+ efflux theory and practice

“…Far from being a passive repository of excess Ca 2+ ions, however, the Ca 2+ content within the SR ([Ca 2+ ] SR ) serves as a critical regulator of the release process itself. Dynamic decreases in local [Ca 2+ ] SR are thought to aid in terminating the elementary units of release, Ca 2+ sparks (Sobie et al, 2002;Terentyev et al, 2002), and, when SR Ca 2+ content is excessive, regenerative release of Ca 2+ is thought to produce arrhythmias (Lederer and Tsien, 1976;Kass et al, 1978;Berlin et al, 1989;Cheng et al, 1996). Here we discuss the balance of influx of Ca 2+ into the SR and its release through Ca 2+ sparks and Ca 2+ "leak".…”