scholarly journals Changes in Membrane Potentials and Currents of Ventricular Cells of the Guinea Pig Heart by a New Cardiotonic Drug, MCI-154

1987 ◽  
Vol 44 (4) ◽  
pp. 481-488
Author(s):  
Sohta KATAYAMA ◽  
Akihiro NARIMATSU ◽  
Reiko SUZUKI ◽  
Toshihiko IIJIMA ◽  
Norio TAIRA
Keyword(s):  
Guinea Pig ◽  
Membrane Potentials ◽  
Guinea Pig Heart ◽  
Ventricular Cells ◽  
Cardiotonic Drug

scholarly journals Changes in membrane potentials and currents of ventricular cells of the guinea pig heart by a new cardiotonic drug, MCI-154.

1987 ◽  
Vol 44 (4) ◽  
pp. 481-488 ◽  
Author(s):  
Sohta KATAYAMA ◽  
Akihiro NARIMATSU ◽  
Reiko SUZUKI ◽  
Toshihiko IIJIMA ◽  
Norio TAIRA
Keyword(s):  
Guinea Pig ◽  
Membrane Potentials ◽  
Guinea Pig Heart ◽  
Ventricular Cells ◽  
Cardiotonic Drug

scholarly journals Involvement of A pertussis Toxin Sensitive G-Protein in the Inhibition of Inwardly Rectifying K+Currents by Platelet-Activating Factor in Guinea-Pig Atrial Cardiomyocytes

1994 ◽  
Vol 3 (1) ◽  
pp. 45-51
Author(s):  
M. Gollasch ◽  
T. Kleppisch ◽  
D. Krautwurst ◽  
D. Lewinsohn ◽  
J. Hescheler
Keyword(s):  
Cyclic Amp ◽  
Guinea Pig ◽  
G Protein ◽  
Pertussis Toxin ◽  
Platelet Activating Factor ◽  
Resting Membrane Potential ◽  
Patch Clamp Technique ◽  
Guinea Pig Heart ◽  
Ventricular Cells ◽  
Inwardly Rectifying

Platelet-activating factor (PAF) inhibits single inwardly rectifying K+channels in guinea-pig ventricular cells. There is currently little information as to the mechanism by which these channels are modulated. The effect of PAF on quasi steady-state inwardly rectifying K+currents (presumably of the IK1type) of auricular, atrial and ventricular cardiomyocytes from guinea-pig were studied. Applying the patch-clamp technique in the whole-cell configuration, PAF (10 nM) reduced the K+currents in all three cell types. The inhibitory effect of PAF occurred within seconds and was reversible upon wash-out. It was almost completely abolished by the PAF receptor antagonist BN 50730. Intracellular infusion of atrial cells with guanine 5′-(β-thio)diphosphate (GDPS) or pretreatment of cells with pertussis toxin abolished the PAF dependent reduction of the currents. Neither extracellularly applied isoproterenol nor intracellularly applied adenosine 3′,5′-cyclic monophosphate (cyclic AMP) attenuated the PAF effect. In multicellular preparations of auricles, PAF (10 nM) induced arrhythmias. The arrhythmogenic activity was also reduced by BN 50730. The data indicate that activated PAF receptors inhibit inwardly rectifying K+currents via a pertussis toxin sensitive G-protein without involvement of a cyclic AMP-dependent step. Since IK1is a major component in stabilizing the resting membrane potential, the observed inhibition of this type of channel could play an important role in PAF dependent arrhythmogenesis in guinea-pig heart.

Palmitoyl-L-carnitine acts like ouabain on voltage, current, and contraction in guinea pig ventricular cells

1995 ◽  
Vol 268 (3) ◽  
pp. H1027-H1036 ◽  
Author(s):  
J. B. Shen ◽  
A. J. Pappano
Keyword(s):  
Guinea Pig ◽  
Ventricular Myocytes ◽  
Present Report ◽  
Ionic Currents ◽  
Pump Current ◽  
Membrane Potentials ◽  
Cell Shortening ◽  
Ventricular Cells ◽  
Ramp Voltage ◽  
Inward Currents

We previously showed that palmitoyl-L-carnitine (L-PC) inhibits the Na/K pump current (INa/K). In the present report, we test the hypothesis that L-PC, like ouabain, should increase myocyte shortening. Membrane potentials or ionic currents were recorded simultaneously with cell shortening in single guinea pig ventricular myocytes at room temperature (22 degrees C). Like ouabain, L-PC (1 microM) reversibly depolarized the resting membrane, decreased action potential duration, and increased the amplitude of myocyte contractions. Neither L-PC nor ouabain had a significant effect on Ca current (ICa). When L-PC increased cell shortening during ramp voltage clamp, membrane current shifted inward at voltages negative to -20 mV and shifted outward at more positive voltages. Similar to toxic concentrations of ouabain, L-PC induced transient inward currents and aftercontractions. At concentrations that inhibit INa/K, L-PC acted like ouabain to produce characteristic effects on membrane potentials, currents, and cell contractions that were unrelated to significant changes in ICa. L-PC reduces surface negative charge of erythrocytes and myocytes (C. Gruver and A. J. Pappano, J. Mol. Cell. Cardiol. 25: 1275–1284, 1993), and we speculate that L-PC inhibits INa/K by this mechanism.

Single cells from adult mammalian heart: Isolation procedure and preliminary electrophysiological studies

1981 ◽  
Vol 59 (8) ◽  
pp. 907-910 ◽  
Author(s):  
J. Omar Bustamante ◽  
Toshifumi Watanabe ◽  
Terence F. McDonald
Keyword(s):  
Guinea Pig ◽  
Single Cells ◽  
Ionic Channel ◽  
Isolation Procedure ◽  
Membrane Properties ◽  
Guinea Pig Heart ◽  
Enzymatic Dissociation ◽  
Ventricular Cells ◽  
Enzyme Method ◽  
Electrophysiological Studies

Single ventricular cells have been isolated from adult guinea pig heart using a collagenase enzyme method. The procedure is straightforward, takes about 20 min, and yields 40–65% rod-shaped cells which are quiescent in millimolar Ca2+ solution. Electrophysiological studies involving external ion changes and ionic channel inhibitors suggest that the cells retain their active membrane properties following this enzymatic dissociation.

scholarly journals Effects of a novel cardioprotective drug JTV-519 on membrane currents of single ventricular cells of the guinea pig heart

1998 ◽  
Vol 76 ◽  
pp. 285
Author(s):  
Junko Kimura ◽  
Masanori Kawahara ◽  
Eiichi Sakai ◽  
Junichi Yatabe ◽  
Hironori Nakanishi
Keyword(s):  
Guinea Pig ◽  
Membrane Currents ◽  
Guinea Pig Heart ◽  
Ventricular Cells ◽  
Cardioprotective Drug

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.

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