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1

Beta-adrenergic stimulation does not influence the activity of lymphocyte Kv1.3 channels

100%
Teisseyre A., Gawlik A., Krasnowska M.
Cellular and Molecular Biology Letters
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1997
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tom 02
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nr 3
The aim of our study was to clarify the still controversial problem concerning the modulatory effect of β-adrenergic stimulation on the activity of Kv1.3 channels in human T Lymphocytes. Because the expression of β-adrenergic receptors in T Lymphocytes is significantly altered in patients with bronchial asthma we examined the cells taken both from healthy donors and asthmatic patients. We applied the whole-cell patch-clamp technique to study the modulatory effect of β-adrenergic stimulation on the whole-cell potassium conductance, gating and kinetics of Lymphocyte Kv1.3 channels. During the experiments β-adrenergic agonist Isoprenaline was applied at concentrations up to 10-4 M. It was shown that the activity of T lymphocyte Kv1.3 channels remain unchanged upon β-adrenergic stimulation both in cells taken healthy donors and asthmatic patients. Results of our investigations support the notion that β- adrenergic stimulation does not modulate the activity of Kv1.3 channels in human TL. The transient increase in T lymphocyte K+ channel activity upon β-adrenergic stimulation that has been reported in some previous studies is most probably due to an activation of recently identified, voltage-independent cAMP-responsive K+ channels.
2
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A synergistic interaction between histamine and vasoactive intestinal peptide [VIP] on cyclic AMP production in the chick pineal gland

100%
Nowak J. Z., Woldan-Tambor A., Kuba K., Zawilska J. B.
Journal of Physiology and Pharmacology
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1998
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tom 49
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nr 3
3
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The aging heart: changes in the pharmacodynamic electrophysiological response to verapamil in aged rabbit hearts

80%
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
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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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