Effects of toquipidine on ionic channels of cultured embryonic Xenopus laevis myoblasts and neurons
Abstract
AIM:
To study the effects of toquipidine (1-p-methyl-phenyl-2-(alpha-piperidinoacetyl)-1, 2, 3, 4-tetrahydroisoquinoline hydrochloride, Toq), a new anti-arrhythmic agent first synthesized in China, on ionic channels.
METHODS:
Ionic channel currents were recorded by whole-cell patch clamp technique in cultured embryonic Xenopus laevis myoblasts and neurons.
RESULTS:
Toq (0.1, 1, 10, and 100 mumol L-1) caused a concentration-dependent inhibition of the Na+ currents with IC50 7.2 mumol L-1 (5.3-9.8 mumol L-1). Toq (10 mumol L-1) also suppressed the high-voltage-activated Ca2+ currents in neurons. But the steady-state outward K+ currents in myoblasts were activated by Toq (10 mumol L-1).
CONCLUSION:
Toq blocked the Na+ and Ca2+ channels and opened the steady-state outward K+ channels.
Keywords:
To study the effects of toquipidine (1-p-methyl-phenyl-2-(alpha-piperidinoacetyl)-1, 2, 3, 4-tetrahydroisoquinoline hydrochloride, Toq), a new anti-arrhythmic agent first synthesized in China, on ionic channels.
METHODS:
Ionic channel currents were recorded by whole-cell patch clamp technique in cultured embryonic Xenopus laevis myoblasts and neurons.
RESULTS:
Toq (0.1, 1, 10, and 100 mumol L-1) caused a concentration-dependent inhibition of the Na+ currents with IC50 7.2 mumol L-1 (5.3-9.8 mumol L-1). Toq (10 mumol L-1) also suppressed the high-voltage-activated Ca2+ currents in neurons. But the steady-state outward K+ currents in myoblasts were activated by Toq (10 mumol L-1).
CONCLUSION:
Toq blocked the Na+ and Ca2+ channels and opened the steady-state outward K+ channels.