Articles |
From the Department of Physiology, Faculty of Medicine, Kyoto (Japan) University.
Correspondence to Dr T. Mitsuiye, Department of Physiology, Faculty of Medicine, Kyoto University, Sakyo-Ku, Kyoto 606, Japan.
Abstract Single ventricular myocytes of guinea
pig heart were distended by applying a positive pressure of 5 to 20
mm Hg in the pipette during the whole-cell voltage clamp. The
amplitude of delayed rectifier K+ current (IK)
was increased by
1.5 times, whereas the inward rectifier
K+ current was scarcely affected. The increase of
IK was reversible by applying a negative pressure of
-10 to -30 mm Hg accompanied by shrinkage of the inflated
cell. This response of IK was largely attributed to the
E-4031insensitive component of IK. The fully
activated current amplitude, measured using long-lasting
depolarizing pulses (>30 seconds) to +60 mV, was increased by the cell
distension. The activation time course of IK during the
long pulse consisted of more than three exponential components, and the
slowest time constant was decreased by the distension from control
20.2±7.7 seconds (n=4) to 7.6±1.6 seconds (n=5).
We failed to detect
an involvement of microtubules or microfilaments, protein kinase C, and
Ca2+ in the inflation-mediated increase of
IK.
Key Words: delayed rectifier K+ current ventricular myocytes guinea pig hearts membrane stretch cytoskeleton
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