We investigated the permeability of Cs+ and Na+
through various ion channels in rat atrial myocytes
using the whole-cell voltage-clamp technique. With
isotonic CsCl (140 mM) on both sides of the membrane
and nominally [Ca2+]o-free conditions, depolarising clamp pulses
induced an increase of outward currents which showed a biphasic time
course. Repolarisation to the holding potential induced inward tail
currents. With isotonic NaCl, depolarisation also induced outward
currents which showed a monotonic decay, but inward tail currents
were not observed. Both in NaCl and CsCl, currents were hardly
affected by TEA (10 mM), 4-AP (5 mM) and DIDS (100 µM).
Nicardipine (1 M) almost completely blocked time-dependent outward
currents in isotonic NaCl solution, leaving only time-independent
currents which showed linear I-V relationship. In isotonic CsCl
conditions, nicardipine blocked outward current considerably, but there
still remained time-dependent outward currents and inward tail
currents. Addition of E-4031 (2-20 M) which is known as a specific
blocker of the rapidly activating delayed rectifier K+ current (IKr)
completely blocked these time-dependent outward and inward currents,
leaving only a time-independent current. Time-independent currents
recorded in the presence of nicardipine and E-4031 were inhibited by
GdCl3, which is known to block non-selective cation (NSC) currents.
From these results, it was suggested that NSC current in atrial myocytes
can be investigated in isotonic Cs+ or Na+ solution in the presence of
Ca2+ channel and IKr blockers.