Cell distension-induced increase of the delayed rectifier K+ current in guinea pig ventricular myocytes

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 (I-K) was increased by approximate to 1.5 times, whereas the inward rectifier K+ current was scarcely affected. The increase of I-K was reversible by applying a negative pressure of -10 to -30 mm Hg accompanied by shrinkage of the inflated cell. This response of I-K was largely attributed to the E-4031-insensitive component of I-K. 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 I-K 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 I-K.