AJP - Heart and Circulatory Physiology, Vol 253, Issue 5 1321-H1324, Copyright © 1987 by American Physiological Society
Intracellular Ca2+ and protein kinase C modulate K+ current in guinea pig heart cells
N. Tohse, M. Kameyama and H. Irisawa
National Institute for Physiological Sciences, Okazaki, Japan.
Effects of protein kinase C (PKC) and intracellular calcium ion (Cai2+) on
the delayed rectifier K+ current (IK) were investigated in the single
ventricular cells of guinea pig by use of an internal-dialysis method and a
whole cell voltage-clamp technique. 12-O-tetradecanoylphorbol-13-acetate
(TPA, 10(-9) M), an activator of PKC, increased the amplitude of IK in the
presence of Cai2+ higher than 10(-10) M. This effect of TPA was mimicked by
a synthetic diacylglycerol, 1-oleoyl-2-acetylglycerol (OAG), 50
micrograms/ml, 125 microM, and was blocked by
1-(5-isoquinolinylsulfonyl)-2-methylpiperazine (10 microM). The above
findings suggest that IK channels were phosphorylated by PKC and thereby
the amplitude of IK was increased. IK was also increased by elevating the
concentration of Cai2+ in the absence of TPA. It is thus indicated that IK
channels are modulated by Cai2+ not only through activation of PKC but also
directly. Our observation may provide a possible mechanism by which Cai2+
mediates the link between the Ca2+ transients during contraction and the
action potential duration.
