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Activation of potassium conductance by ophiopogonin‐D in acutely dissociated rat paratracheal neurones
Author(s) -
Ishibashi Hitoshi,
Mochidome Takanobu,
Okai Junpei,
Ichiki Hiroyuki,
Shimada Hideaki,
Takahama Kazuo
Publication year - 2001
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1038/sj.bjp.0703818
Subject(s) - apamin , tetraethylammonium , charybdotoxin , reversal potential , chemistry , membrane potential , depolarization , glibenclamide , biophysics , potassium channel , tetraethylammonium chloride , repolarization , channel blocker , patch clamp , potassium channel blocker , electrophysiology , endocrinology , medicine , potassium , calcium , biology , biochemistry , organic chemistry , diabetes mellitus
The effect of ophiopogonin‐D (OP‐D), a steroidal glycoside and an active component of Bakumondo‐to, a Chinese herbal antitussive, on neurones acutely dissociated from paratracheal ganglia of 2‐week‐old Wistar rats was investigated using the nystatin‐perforated patch recording configuration. Under current‐clamp conditions, OP‐D (10 μ M ) hyperpolarized the paratracheal neurones from a resting membrane potential of −65.7 to −73.5 mV. At the concentration of 1 μ M and above, OP‐D concentration‐dependently activated an outward current accompanied by an increase in the membrane conductance under voltage‐clamp conditions at a holding potential of −40 mV. The reversal potential of the OP‐D‐induced current (I OP‐D ) was −79.4 mV, which is close to the K + equilibrium potential of −86.4 mV. The changes in the reversal potential for a 10 fold change in extracellular K + concentration was 53.1 mV, indicating that the current was carried by K + . The I OP‐D was blocked by an extracellular application of 1 m M Ba 2+ by 59.0%, but other K + channel blockers, including 4‐aminopyridine (3 m M ), apamin (1 μ M ), charybdotoxin (0.3 μ M ), glibenclamide (1 μ M ), tolbutamide (0.3 m M ) and tetraethylammonium (10 m M ), did not inhibit the I OP‐D . OP‐D also inhibited the ACh‐ and bradykinin‐induced depolarizing responses which were accompanied with firing of action potentials. The results suggest that OP‐D may be of benefit in reducing the excitability of airway parasympathetic ganglion neurones and consequently cholinergic control of airway function and further, that the hyperpolarizing effect of OP‐D on paratracheal neurones via an activation of K + channels might explain a part of mechanisms of the antitussive action of the agent.British Journal of Pharmacology (2001) 132 , 461–466; doi: 10.1038/sj.bjp.0703818