Rutaecarpine-induced block of delayed rectifier K+ current in NG108-15 neuronal cells

@article{Wu2001RutaecarpineinducedBO,
  title={Rutaecarpine-induced block of delayed rectifier K+ current in NG108-15 neuronal cells},
  author={Sheng-Nan Wu and Y K Lo and Hsinyo Chen and Hui-fang Li and Hung Ting Chiang},
  journal={Neuropharmacology},
  year={2001},
  volume={41},
  pages={834-843}
}
The effects of rutaecarpine on ionic currents of NG108-15 neuronal cells were investigated in this study. Rutaecarpine (2-100 microM) suppressed the amplitude of delayed rectifier K+ current (I(K(DR))) in a concentration-dependent manner. The IC50 value for rutaecarpine-induced inhibition of I(K(DR)) was 11 microM. I(K(DR)) present in these cells is sensitive to the inhibition by quinidine and dendrotoxin, yet not by E-4031. The presence of rutaecarpine enhanced the rate and extent of I(K(DR… Expand
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References

SHOWING 1-10 OF 25 REFERENCES
New channel blocker BIIA388CL blocks delayed rectifier, but not A-type potassium current in central neurons
TLDR
BIIA388Cl is an effective and selective blocker of I(DR), the main pathway for the loss of intracellular potassium by depolarized neurons, which could be useful for neuroprotection. Expand
Characterization of Inhibition by Risperidone of the Inwardly Rectifying K+ Current in Pituitary GH3 Cells
TLDR
Evidence is provided that risperidone, in addition to the blockade of dopamine receptors, can produce a depressant effect on IK(IR) and BKCa channels, and implies that the blockadeOf these ionic currents by ris peridone may affect membrane excitability and prolactin secretion in GH3 cells. Expand
Block by capsaicin of voltage‐gated K+ currents in melanotrophs of the rat pituitary
  • S. J. Kehl
  • Chemistry, Medicine
  • British journal of pharmacology
  • 1994
TLDR
Most of the effects of capsaicin on the IK(s) of melanotrophs can be accounted for by a kinetic scheme in which Capsaicin binds to and blocks open K+ channels. Expand
Inactivation of the ERG current in NG108-15 cells.
  • H. Meves
  • Chemistry, Medicine
  • Biochemical and biophysical research communications
  • 1999
TLDR
The curve relating time constant of inactivation tau to membrane potential V could be fitted by a Gauss curve and resembles the relation between tau and [K(+)](o) in ERG channels expressed in Xenopus oocytes. Expand
The vasorelaxing action of rutaecarpine: direct paradoxical effects on intracellular calcium concentration of vascular smooth muscle and endothelial cells.
TLDR
The paradoxical regulation of Ca++ in both VSMC and EC acts simultaneously to cause vasorelaxation which could account, at least in part, for the hypotensive action. Expand
Ionic mechanisms responsible for the antiarrhythmic action of dehydroevodiamine in guinea‐pig isolated cardiomyocytes
TLDR
The present findings indicate that DeHE may depress triggered arrhythmias in Ca‐overloaded guinea‐pig cardiac myocytes through its inhibitory actions on INa, Iti and, to a smaller extent, ICa. Expand
The characteristics in the inhibitory effects of capsaicin on voltage-dependent K(+) currents in rat atrial myocytes.
TLDR
The present findings suggest that in isolated rat atria, during Capsaicin exposure, the capsaicin-mediated inhibition of these K(+) channels is one of the ionic mechanisms underlying the positive inotropic and chronotropic actions. Expand
Effect of capsaicin on membrane currents in cultured vascular smooth muscle cells of rat aorta.
TLDR
Results suggest that inhibition of the voltage-dependent L-type Ca2+ channel is involved in the capsaicin-induced relaxation of the vascular smooth muscle, whereas capsaicIn-induced inhibition of voltage- dependent K+ channels might produce an increase in cell excitability. Expand
Studies of the cellular mechanisms underlying the vasorelaxant effects of rutaecarpine, a bioactive component extracted from an herbal drug.
TLDR
Results suggest that these vasorelaxants had different cellular mechanisms and that neither pertussis toxin-sensitive Gi protein, other G proteins, nor phospholipase C activation was involved in the cellular response to rutaecarpine. Expand
Mechanism of inhibition of platelet aggregation by rutaecarpine, an alkaloid isolated from Evodia rutaecarpa.
TLDR
It is concluded that the antiplatelet effects of rutaecarpine are due to inhibition of thromboxane formation and phosphoinositide breakdown. Expand
...
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