scholarly journals Inward rectifier K + current under physiological cytoplasmic conditions in guinea‐pig cardiac ventricular cells

2002 ◽  
Vol 540 (3) ◽  
pp. 831-841 ◽  
Author(s):  
Keiko Ishihara ◽  
Ding‐Hong Yan ◽  
Shintaro Yamamoto ◽  
Tsuguhisa Ehara
Keyword(s):  
Guinea Pig ◽  
Inward Rectifier ◽  
Ventricular Cells ◽  
K Current

Endothelin-1 Partially Inhibits ATP-Sensitive K+ Current in Guinea Pig Ventricular Cells

1996 ◽  
Vol 27 (1) ◽  
pp. 12-19 ◽  
Author(s):  
Satoru Kobayashi ◽  
Haruaki Nakaya ◽  
Taichi Takizawa ◽  
Yukio Hara ◽  
Sadao Kimura ◽  
...  
Keyword(s):  
Guinea Pig ◽  
Endothelin 1 ◽  
Ventricular Cells ◽  
K Current

Intracellular Ca2+ and protein kinase C modulate K+ current in guinea pig heart cells

1987 ◽  
Vol 253 (5) ◽  
pp. H1321-H1324 ◽  
Author(s):  
N. Tohse ◽  
M. Kameyama ◽  
H. Irisawa
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Guinea Pig ◽  
Cell Voltage ◽  
Delayed Rectifier ◽  
Heart Cells ◽  
Guinea Pig Heart ◽  
Kinase C ◽  
Ventricular Cells ◽  
K Current

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.

Calcium-sensitive delayed rectifier potassium current in guinea pig ventricular cells

1990 ◽  
Vol 258 (4) ◽  
pp. H1200-H1207 ◽  
Author(s):  
N. Tohse
Keyword(s):  
Guinea Pig ◽  
Noise Analysis ◽  
Cardiac Cells ◽  
Delayed Rectifier ◽  
Activation Process ◽  
Patch Clamp Technique ◽  
Open Probability ◽  
Activation Curve ◽  
Ventricular Cells ◽  
K Current

The calcium sensitivity of the delayed rectifier K+ current (IK) was investigated in guinea pig single ventricular cells using the whole cell configuration of the patch-clamp technique with a cell dialysis method. The concentration-response curve of IK for intracellular Ca2+ indicated that IK started to increase at intracellular Ca2+ concentration [Ca2+]i of 10(-8) M (pCa 8) and it increased threefold at pCa 7. At lower [Ca2+]i than pCa 9, IK remained unchanged. A shift of the activation curve of IK by the elevation of [Ca2+]i was not observed. Although [Ca2+]i had little effect on time constants of the activation and deactivation of IK, it predominantly increased the amplitudes of the fast components in the activation process and the slow component in the deactivation process. In the ensemble noise analysis, the elevation of [Ca2+]i increased the number and open probability of functional IK channels but not the unit amplitude of IK channel. These results suggest that the elevation of [Ca2+]i enhances IK, probably by increasing the number and open probability of functional IK channels. Ca2(+)-sensitive IK in cardiac cells is a class of current different from Ca2(+)-activated K+ current in other tissue because the activation curve of Ca2(+)-sensitive IK was not shifted by the [Ca2+]i elevation, and the single channel conductance of IK was smaller than the one of Ca2(+)-activated K+ current.

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