Blockade of sodium and potassium channels in the node of Ranvier by ajmaline and N-propyl ajmaline.

Article Details

Citation

Copy to clipboard

Khodorov BI, Zaborovskaya LD

Blockade of sodium and potassium channels in the node of Ranvier by ajmaline and N-propyl ajmaline.

Gen Physiol Biophys. 1983 Aug;2(4):233-68.

PubMed ID

6088360 [ View in PubMed

]

Abstract

The inhibition of sodium and potassium currents in frog myelinated fibres by ajmaline (AM) and its quaternary derivative, N-propyl ajmaline (NPA), depends on voltage-clamp pulses and the state of channel gating mechanisms. The permanently charged NPA and protonated AM interact only (or mainly) with open channels, while unprotonated AM affects preferently inactivated Na channels. Inhibition of Na currents by NPA and AM does not depend on the current direction and Na ion concentration in external or internal media. In contrast only the outward potassium currents can be blocked by NPA and AM; the inward potassium currents in high K+ ions external media are resistant to the blocking action of these drugs. The voltage dependence of ionic current inhibition by charged drugs suggests the location of their binding sites in the inner mouths of Na and K channels. Judging by the kinetics of current restoration after cessation of pulsing, the drug-binding site complex is much more stable in Na than in potassium channels. Batrachotoxin and aconitine, unlike veratridine and sea anemone toxin, decrease greatly the affinity of Na channel binding sites to NPA and AM. The effects of NPA and AM are compared with those of local anesthetics and other amine blocking drugs.

DrugBank Data that Cites this Article

Drug Targets

Drug	Target	Kind	Organism	Pharmacological Action	Actions
Ajmaline	Sodium channel protein type 5 subunit alpha	Protein	Humans	Yes	Inhibitor	Details