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 approximately 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).
Wang
Z
Z
Department of Physiology, Faculty of Medicine, Kyoto University, Japan.
Mitsuiye
T
T
Noma
A
A
D000200:Action Potentials; D000818:Animals; D002478:Cells, Cultured; D003599:Cytoskeleton / Q000502:physiology; D006168:Guinea Pigs; D006321:Heart / Q000502:physiology*; D006352:Heart Ventricles / Q000166:cytology; D009206:Myocardium / Q000166:cytology* / Q000378:metabolism; D015221:Potassium Channels / Q000502:physiology*; D016276:Ventricular Function
D015221:Potassium Channels