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1
Content available remote

The human ether-a-go-go-related gene (hERG) current inhibition selectively prolongs action potential of midmyocardial cells to augment transmural dispersion

100%
Yasuda C., Yasuda S., Yamashita H., Okada J., Hisada T., Sugiura S.
Journal of Physiology and Pharmacology
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2015
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tom 66
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nr 4
2

Characteristics of anion and SV channels in the vacuoles of the liverwort Conocephalum conicum L.

86%
Dziubinska H., Krol E., Hanaka A., Trebacz K.
Polish Journal of Natural Sciences. Supplement
|
2003
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tom 01
3

The characteristics of anion channels in the tonoplast of the liverwort Conocephalum conicum. A patch-clamp study

86%
Dziubinska H., Hanaka A., Krol E., Trebacz K.
Cellular and Molecular Biology Letters
|
2002
|
tom 07
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nr Suppl.
4
Content available remote

Influence of the multidrug transporter inhibitors on the activity of Kv1.3 voltage-gated potassium channels

72%
Teisseyre A., Duarte N., Ferreira M.-J. U., Michalak K.
Journal of Physiology and Pharmacology
|
2009
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tom 60
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nr 1
69-76
Using the whole-cell patch-clamp technique, the influence of selected multidrug resistance modulators, both plant-derived compounds and derivatives on the activity of voltage-gated potassium channels Kv1.3 was investigated. Twelve compounds with phenolic and terpenic structures were tested: the stilbenes piceatannol (1) and its tetramethoxy (2) and tetracetoxy (3) derivatives, the flavonoids naringenin (4) and its methylated derivatives: naringenin-4',7-dimethylether (5) and naringenin-7-methylether (6), and aromadendrin (7), the coumarins esculetin (8) and scopoletin (9) and ent-abietane diterpenes, helioscopinolide B (10) and its 3ß-acetoxy derivative (11) and helioscopinolide E (12). The studies were performed on a model system with Kv1.3 channels endogenously expressed in human T lymphocytes. Obtained data provide evidence that compounds 2, 5 and 6 applied at 30 µM inhibited the amplitude of recorded currents to 31%, 4% and 29% of its control value, respectively. On the other hand, compounds 3, 4, 7-12 (at 30 µM) and compound 1 (at 40 µM) did not affect significantly the channel activity. These results indicate that some methoxy-derivatives of the tested compounds are effective inhibitors of Kv1.3 channels. Since the inhibition of Kv1.3 channels may inhibit the proliferation of prostate, breast and colon cancer cells expressing these channels, the channel inhibitors may exert an antiproliferative action. This action combined with a simultaneous modulation of the multidrug resistance may be significant for a potential application of these compounds in cancer chemotherapy.
5

The influence of protons and zinc ions on the steady-state inactivation of Kv1.3 potassium channels

72%
Teisseyre A., Mozrzymas J. W.
Cellular and Molecular Biology Letters
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2007
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tom 12
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nr 2
Using the whole-cell patch-clamp technique, we investigated the influence of extracellular pH and zinc ions (Zn2+) on the steady-state inactivation of Kv1.3 channels expressed in human lymphocytes. The obtained data showed that lowering the extracellular pH from 7.35 to 6.8 shifted the inactivation midpoint (Vi) by 17.4 ± 1.12 mV (n = 6) towards positive membrane potentials. This shift was statistically significant (p < 0.05). Applying 100 μM Zn2+ at pH 6.8 further shifted the Vi value by 16.55 ± 1.80 mV (n = 6) towards positive membrane potentials. This shift was also statistically significant (p < 0.05). The total shift of the Vi by protons and Zn2+ was 33.95 ± 1.90 mV (n = 6), which was significantly higher (p < 0.05) than the shift caused by Zn2+ alone. The Zn2+-induced shift of the Vi at pH 6.8 was almost identical to the shift at pH = 7.35. Thus, the proton-and Zn2+-induced shifts of the Vi value were additive. The steady-state inactivation curves as a function of membrane voltage were compared with the functions of the steady-state activation. The total shift of the steady-state inactivation was almost identical to the total shift of the steady-state activation (32.01 ± 2.10 mV, n = 10). As a result, the “windows” of membrane potentials in which the channels can be active under physiological conditions were also markedly shifted towards positive membrane potentials. The values of membrane voltage and the normalised chord conductance corresponding to the points of intersection of the curves of steady-state activation and inactivation were also calculated. The possible physiological significance of the observed modulatory effects is discussed herein.
6
Content available remote

The aging heart: changes in the pharmacodynamic electrophysiological response to verapamil in aged rabbit hearts

58%
Salameh A., Dhein S., Fleischmann B., Grohe C., Hescheler J., Linz K. W., Meyer R.
Journal of Physiology and Pharmacology
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2010
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tom 61
|
nr 2
The aim of this study was to investigate whether the L-type calcium current (ICa.L) may be altered in aged hearts and whether the classical calcium antagonist verapamil may exhibit altered pharmacological profile in aged hearts. We examined male New Zealand rabbits aged either 6 months or 26 months. To examine ICa.L whole-cell patch-clamp technique was performed on isolated cells. Moreover, activation-recovery intervals (ARI) of isolated hearts (Langendorff method) were assessed using an epicardial 256 channel mapping system. We found that the ICa.L density, normalised to the cell volume was significantly reduced (p<0.001). Maximum conductance was also significantly decreased (p=0.01) and steady state inactivation was shifted to more positive potentials in aged hearts (p<0.001). A slightly reduced effect of ß-adrenergic modulation of the ICa.L in aged hearts, and a significantly reduced effect of carbachol on isoprenaline-stimulated ICa.L in aged hearts was observed. L-type 1c subunit, SERCA2-ATPase and the Na+/Ca2+-exchanger expression were neither significantly different in atrial and ventricular tissues nor between young and old animals. Using the mapping system, isolated hearts were exposed to verapamil (0.005, 0.01, 0.02, 0.05 µM/L). While verapamil did not affect ARI in young hearts, in aged hearts ARI was concentration-dependently reduced and the negative inotropic effect of verapamil was significantly attenuated in aged hearts (p<0.05). From these results we conclude that there are distinct alterations in the electrophysiology of ICa.L (reduced maximum conductance, a shift of the steady state inactivation) in the aged heart which may influence the response to verapamil.
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