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J Vereecke

Publications and source records attributed to J Vereecke.

At least 55 records · Page 3Linked to original sources
PubMed1989

Subconductance states in cardiac sodium channels.

Single Na channel currents were studied in cell-attached patches from guinea-pig ventricular myocytes in the presence of DPI 201-106. In addition to openings with a single channel conductance of 15 pS, two other types of events occur that are characterized by a conductance of 5 and 8 pS. The low conductance state is less sensitive to block by TTX than the higher conductance states. The medium conductance state has a reversal potential which is similar to the high conductance channel. It is argued that the low conductance channel is a second type of Na channel, whereas the medium conductance channel appears to be a low conductance substate of the normal Na channels.

Animals↗
PubMed1989

Effect of external K on the block of the inward rectifier during hyperpolarization in guinea-pig ventricular myocytes by external Na.

The effect of changes of the external K concentration on the block of the inward-rectifying K current during hyperpolarization in guinea-pig ventricular myocytes by external Na was investigated. The voltage-dependent block of iK1 by external Na ions is decreased when the external K concentration is lowered between 5.4 and 0.54 mM, but is not influenced when Ko is increased from 5.4 to 27 mM. The effect of lowering Ko can be described as a decrease of the rate of entry of blocking Na ions at lower external K.

Animals↗
PubMed1988

Differential effects of verapamil and flunarizine on cardiac L-type and T-type Ca channels.

Whole cell experiments were used to study whether the L-type and the T-type Ca channel in guinea-pig ventricular myocytes are blocked similarly by verapamil and flunarizine. The L-type current is blocked by 5 mumol/l verapamil and 5 mumol/flunarizine in a use-dependent way, and block can be relieved by hyperpolarizing pulses in a potential-dependent way. The T-type current is not affected by 10 mumol/l verapamil while it is blocked by 10 mumol/l flunarizine in a use-dependent way. Verapamil selectively blocks the L-type channel in contrast to flunarizine.

Animals↗
PubMed1988

The T-type Ca channel in guinea-pig ventricular myocytes is insensitive to isoproterenol.

Whole cell clamp experiments and single channel measurements were used to study whether the T-type Ca channel in guinea-pig ventricular myocytes is sensitive to beta-adrenergic stimulation. In whole cell clamp experiments we determined the T-type Ca current by measuring the difference between the currents at a test potential of -30 mV in Na-free solution, starting from a holding potential either at -90 or at -50 mV. Application of 1 microM isoproterenol (ISO) did not change the difference current, while the L-type Ca current was enhanced during application of the drug. In cell attached patch experiments with 110 mM CaCl2 in the pipette solution, single channel currents were observed which were due to opening of the T-type Ca channel. Application of 4 microM ISO to the bath solution did neither change the appearance of the channel openings, nor the ensemble averaged currents. It is concluded that the T-type Ca channel in guinea-pig ventricular cells is insensitive to ISO.

Animals↗
PubMed1988

The effect of inhibition of mitochondrial energy metabolism on the transient inward current of isolated guinea-pig ventricular myocytes.

Delayed afterdepolarizations (DADs) might underlie ischemic or reperfusion arrhythmias (Ferrier et al., 1985; Coetzee and Opie, 1987). These DADs are the result of a transient inward current iti, which is caused by instability of the intracellular level of free Ca2+ (Cai) due to an oscillatory release of Ca from the sarcoplasmic reticulum (Kass et al., 1978). DADs are known to be abolished by hypoxia and by metabolic inhibition (Di Gennaro et al., 1987; Coetzee and Opie, 1987), which could be caused by a number of different mechanisms: (1) The large increase of potassium conductance associated with metabolic inhibition (Vleugels et al., 1980; Isenberg et al., 1983) could prevent iti from causing a marked depolarization, and would thus "mask" the DADS. (2) Although metabolic inhibition will eventually result in an increase of Cai, a temporary decrease could initially take place, thereby minimizing the Ca instability. Two mechanisms are known which might produce such an effect: Firstly, the shortening of the action potential which occurs during metabolic inhibition will markedly reduce the time during which Ca channels remain open, thereby causing a diminished total Ca influx during the action potential (Isenberg et al., 1983; Noma and Shibasaki, 1985; Kakei et al., 1985). Secondly, a direct reduction of iCa by a decrease in ATP concentration, described by Irisawa and Kokubun (1983), could also contribute to a decreased Ca load. (3) Metabolic inhibitors could possibly interfere with the cycling of Ca between different compartments within the cell, thereby altering the temporal variation in Cai, and thus influencing iti.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1987

Potassium currents in cardiac cells.

The kinetic properties of the inwardly rectifying K current and the transient outward current in cardiac cells were investigated. In sheep Purkinje fibers superfused with Na-free K-free solution, time-dependent changes in the conductance of the inward rectifier are described. In patch clamp experiments the inward rectifier inactivates during hyperpolarization, as can be seen by a decrease in the open state probability. Using whole cell clamp on ventricular myocytes it is demonstrated that the inactivation during hyperpolarization is due to blocking of the channel by external Na, Mg and Ca. The channels responsible for the transient outward current in cow, sheep and rabbit Purkinje fibers are identified using single channel recording. It is demonstrated that in all three preparations the channels are K-selective. The channel in cow Purkinje cells has a large conductance and is regulated by voltage and internal Ca concentration. The channels identified in the sheep and rabbit cells have a much smaller conductance.

Animals↗
PubMed1987

The mechanism of the inactivation of the inward-rectifying K current during hyperpolarizing steps in guinea-pig ventricular myocytes.

The time course of the inward-rectifying K current during hyperpolarizing clamp steps was investigated in single myocytes isolated from guinea-pig ventricles. The experiments were done using a two-electrode voltage-clamp technique with two patch pipettes in the whole-cell configuration. Hyperpolarizations to potentials negative to -100 mV, induced large inward-rectifying K currents (iK1), which showed a marked decay. The current-voltage relation of the peak inward current was almost linear, but the steady-state current-voltage relation had a region of negative slope at potentials negative to -140 mV. These findings indicate that the channel inactivates during hyperpolarizing steps. When Na ions in the extracellular solution were replaced by choline, Tris, TMA or sucrose, the decay of the inward currents was largely reduced, and the negative slope in the steady-state current-voltage relation was absent. When divalent ions were removed from the Na-free bathing solution, a marked increase in iK1 was found, and the currents became time-independent. These experiments demonstrate that the inactivation during hyperpolarization is largely due to a block of the channel by external Na ions. The block by Na is most pronounced at very negative potentials, and is strongly voltage-dependent. External Ca and Mg ions also cause a marked block of the channel. The block by these divalent ions is however much less voltage-dependent than the one by Na, but is already present at the cell's resting potential.

Animals↗
PubMed1987

The electrophysiological effects of acetylcholine in single human atrial cells.

Single cells were isolated from human atria. The ionic currents in these cells were measured using the whole cell clamp technique. Time-dependent currents during depolarizing clamp steps can be described as due to Ca current and transient outward current. Time-dependent inward currents were seen during hyperpolarizing voltage steps. These currents are carried by the inward rectifier iK1, while in some cells also an if pacemaker current is present. The effect of acetylcholine was investigated at potentials negative to -50 mV. Acetylcholine induces an inwardly rectifying K current. The acetylcholine-induced current is different from iK1 in kinetics and Ba-sensitivity. The effect of acetylcholine decreases in time due to desensitization. The electrical response of the human atrial cells to acetylcholine is qualitatively similar to the effect of acetylcholine in guinea-pig atrial cells.

Acetylcholine↗
PubMed1986

Existence of a calcium-dependent potassium channel in the membrane of cow cardiac Purkinje cells.

Single-channel currents were recorded in the membrane of cow cardiac Purkinje cells using the patch-clamp technique. Recordings from cell-attached and cell-free patches demonstrated large outward single-channel currents associated with depolarizing voltage-clamp pulses. The time course of the reconstructed mean current showed a rapid activation phase followed by a slower inactivation following a single exponential time course with a time-constant in the range 30 ms to 100 ms. The current-voltage relation of the channel was linear in the voltage range between +10 mV and +110 mV with a slope conductance of 120 pS in 10.8 mM external K. The results indicated that the channel is selective for K ions. In inside-out patches, when the internal Ca activity was raised from 0.01 microM to 1 microM, the frequency of opening of the K channel during a depolarizing pulse was markedly increased, indicating Ca-dependence of these channels. The relation between this ion channel and the previously described transient outward current in cow Purkinje fibres is discussed. In sheep Purkinje cells a channel, carrying a transient outward current, with different properties was found.

Animals↗
PubMed1986

Electrophysiological effects of tetracaine in single guinea-pig ventricular myocytes.

The effect of tetracaine on the ionic current in enzymatically dissociated single guinea-pig ventricular cells was studied using a two micro-electrode voltage-clamp technique. The myocytes were pre-incubated with Cs+ and the experiments were performed at room temperature in order to reduce the contribution of the delayed outward current. Tetracaine decreased the maximum rate of rise of the action potential with a dissociation constant (KD) strongly dependent on the holding potential (0.77 microM at -80 mV, and 6.2 microM at -95 mV). Application of 20 microM-tetracaine resulted in about a 50% reduction of the inwardly rectifying K+ current, while ten times higher concentrations were required to suppress the delayed K+ current. The inactivation time course of the Ca2+ current could be fitted with two exponentials, with time constants tau f = 15 ms and tau s = 150 ms at around 0 mV. Tetracaine decreased the amplitude of the Ca2+ current and speeded its decay. This effect was found to be primarily due to a marked inhibition of the amplitude of the slowly inactivating component (apparent KD = 80 microM, nH = 2). The drug had little effect on the time constants of the two components of Ca2+ channel inactivation. When Sr2+ or Ba2+ were the charge carriers, inactivation of the Ca2+ channel was again fitted with a fast and a slow exponential. In addition, a maintained (or very slowly inactivating) component was present. Tetracaine not only suppressed the amplitudes of the slowly inactivating and the maintained components, but also decreased the time constant of the slowly inactivating component. The results are consistent with a direct effect of tetracaine on the high threshold Ca2+ channel and do not support indirect effects of the drug secondary to suppression of Ca2+ release from internal stores.

Action Potentials↗
PubMed1984

Single cardiac Purkinje cells: general electrophysiology and voltage-clamp analysis of the pace-maker current.

Single Purkinje cells from dog, sheep and cow hearts were isolated by injecting a Ca-free collagenase containing Tyrode solution in the space between the connective tissue sheath and the Purkinje cells. A small proportion of these cells survived the isolation procedure and these cells were used for further investigation. The cells showed electrophysiological properties similar to intact Purkinje fibres as indicated by the following results. Maximum diastolic potentials between -70 and -85 mV and specific membrane resistances of 21-32 k omega cm2 indicated that the single cells were not leaky or hyperpermeable . The action potential showed a rapid upstroke, with a maximum rate of rise, Vmax' between 150 and 750 V/s, and two phases of fast repolarization separated by a plateau phase with a duration of about 200 ms. Each action potential was followed by a spontaneous depolarization with an amplitude between 1 and 10 mV. The upstroke of the action potential could be blocked by tetrodotoxin (TTX) in a dose-dependent manner. The rate of depolarization of the action potential was sensitive to changes in membrane potential; the resulting S-shaped curve showed a half-maximum potential of -65 mV and a steepness of 0.46 mV-1. The duration of the action potential was sensitive to external K concentrations, catecholamines and TTX in a way similar to intact Purkinje fibres. Both application of catecholamines and lowering the external K concentration induced spontaneous activity. The cells were used to study the ionic nature of the pace-maker current under voltage-clamp conditions using the two-micro-electrode technique. This pace-maker current was blocked in a voltage-dependent manner by 1 mM-Cs, and was not affected by 1 mM-Ba. The steady-state activation curve was shifted in the depolarizing direction by application of adrenaline. In contrast to voltage-clamp data obtained on the pace-maker current of intact Purkinje fibres, the pace-maker current in a single cell did not reverse near the presumed equilibrium potential for K ions; no reversal could be seen in the voltage range negative to -50 mV. These observations together with preliminary results on the Na and K dependence of the pace-maker current are strong arguments in favour of the hypothesis that the pace-maker current in cardiac Purkinje fibres is an inward current carried by Na and K ions and activates upon hyperpolarization.

Action Potentials↗