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School of Biomedical Sciences, University of Leeds, Leeds LS2 9JT, United Kingdom
The effect
of acidosis on the transient outward K+ current
(Ito) of rat ventricular myocytes has been
investigated using the perforated patch-clamp technique. When the
holding potential was
80 mV, depolarizing pulses to potentials
positive to
20 mV activated Ito in
subepicardial cells but activated little Ito in
subendocardial cells. Exposure to an acid solution (pH 6.5) had no
significant effect on Ito activated from this
holding potential in either subepicardial or subendocardial cells. When
the holding potential was
40 mV, acidosis significantly
increased Ito at potentials positive to
20
mV in subepicardial cells but had little effect on
Ito in subendocardial cells. The increase in
Ito in subepicardial cells was inhibited by 10 mM
4-aminopyridine. In subepicardial cells, acidosis caused a +8.57-mV
shift in the steady-state inactivation curve. It is concluded that in
subepicardial rat ventricular myocytes acidosis increases the amplitude
of Ito as a consequence of a depolarizing shift in
the voltage dependence of inactivation.
heart; cardiac electrophysiology; subepicardium; subendocardium
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