Sodium conductance in calcium channels of guinea-pig ventricular cells induced by removal of external calcium ions

1986 ◽  
Vol 407 (5) ◽  
pp. 465-475 ◽  
Author(s):  
Hiroko Matsuda
Keyword(s):  
Guinea Pig ◽  
Calcium Channels ◽  
Calcium Ions ◽  
Sodium Conductance ◽  
Ventricular Cells ◽  
External Calcium

Ionic diffusion in transverse tubules of cardiac ventricular myocytes

1998 ◽  
Vol 275 (3) ◽  
pp. H852-H860 ◽  
Author(s):  
Neal Shepherd ◽  
Holly B. McDonough
Keyword(s):  
Guinea Pig ◽  
Calcium Ions ◽  
Rate Of Change ◽  
Slow Phase ◽  
Total Current ◽  
Transverse Tubules ◽  
Current Increase ◽  
Atrial Cells ◽  
Ventricular Cells ◽  
Current Change

We have estimated the rate of diffusion of calcium ions in the transverse tubules of isolated cardiocytes by recording changes in peak calcium current ( I Ca) caused by rapid changes of the extracellular calcium concentration ([Ca]o) at various intervals just preceding activation of I Ca. Isolated ventricular cells of guinea pig heart and atrial cells from rabbit heart were voltage-clamped (whole cell patch), superfused at a high flow rate, and stimulated continuously with depolarizing pulses (0.5 Hz, 200- or 20-ms pulses from a holding potential of −45 or −75 mV to 0 mV). In ventricular cells, the change in peak I Ca following a sudden change of [Ca]oincreased rapidly as the delay between the solution change and depolarization was increased, up to a delay of ∼75 ms [time constant (τ) ≈ 20 ms, 30–40% of total current change), and then increased more slowly (τ ≈ 200 ms, 60–70% of total current change); 400–500 ms were needed to achieve 90% of the total current increase. In atrial cells, a clear separation into two phases was not possible and 90% of the current change occurred within 85 ms. The slow phase of current change, which was unique to the ventricular cells, presumably reflects the slow equilibration of ions between the bulk perfusate and the lumina of the transverse tubules. If the lengths of the transverse tubules were equal to the cell thickness, the slow rate of change of current would be consistent with an apparent diffusion coefficient for calcium ions of 0.95 × 10−6cm2/s, considerably smaller than the value in bulk solution (7.9 × 10−6cm2/s). Most likely, this discrepancy is due to a high degree of tortuosity in the transverse tubular system in guinea pig ventricular cells or possibly to ion binding sites within the tubular membranes and glycocalyx.

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.

Histamine-operated calcium channels in intestinal smooth muscle of the guinea-pig

1987 ◽  
Vol 135 (1) ◽  
pp. 69-75 ◽  
Author(s):  
Nicole Morel ◽  
Jean-Paul Hardy ◽  
Théophile Godfraind
Keyword(s):  
Smooth Muscle ◽  
Guinea Pig ◽  
Calcium Channels ◽  
Intestinal Smooth Muscle

Properties and distribution of single voltage-gated calcium channels in adult hippocampal neurons

1990 ◽  
Vol 64 (1) ◽  
pp. 91-104 ◽  
Author(s):  
R. E. Fisher ◽  
R. Gray ◽  
D. Johnston
Keyword(s):  
Guinea Pig ◽  
Calcium Channels ◽  
Single Channel ◽  
Cell Types ◽  
Voltage Gated ◽  
Channel Current ◽  
Single Channel Current ◽  
Voltage Gated Calcium Channels ◽  
Large Conductance Channel ◽  
Small Conductance

1. The properties of single voltage-gated calcium channels were investigated in acutely exposed CA3 and CA1 pyramidal neurons and granule cells of area dentata in the adult guinea pig hippocampal formation. 2. Guinea pig hippocampal slices were prepared in a conventional manner, then treated with proteolytic enzymes and gently shaken to expose the somata of the three cell types studied. Standard patch-clamp techniques were used to record current flow through calcium channels in cell-attached membrane patches with isotonic barium as the charge carrier. 3. Single-channel current amplitudes were measured at different membrane potentials. Single-channel current-voltage plots were constructed and single-channel slope conductances were found to fall into three classes. These were (approximately) 8, 14, and 25 pS, and were observed in all three cell types. 4. The three groups of channels differed from each other in voltage dependence of activation: from a holding potential of -80, the small-conductance channel began to activate at about -40 to -30 mV, the medium-conductance channel at about -20 mV, and the large-conductance channel at approximately 0 mV. 5. Ensemble averages of single-channel currents during voltage steps revealed differences in voltage-dependent inactivation. The small-conductance channel inactivated completely within approximately 50 ms during steps from -80 to -10 mV or more positive. Steps to less positive potentials resulted in less inactivation. The medium-conductance channel displayed variable inactivation during steps from -80 to 0 mV. Inactivation of this channel during a 160-ms step ranged from virtually zero to approximately 100%. The large-conductance channel displayed no significant inactivation during steps as long as 400 ms. 6. The large-conductance channel was strikingly affected by the dihydropyridine agonist Bay K8644 (0.5-2.0 microM), resulting in a high probability of channel opening, prolonged openings, and an apparent increase in the number of channels available for activation. The medium and small-conductance channels were not noticeably affected by the drug. 7. The large-conductance channel could be induced to open at very negative membrane potentials by holding the patch for several seconds at 20 or 30 mV and stepping to -30 or -40 mV. This process was enhanced by Bay K8644, resulting in prolonged openings at potentials as negative as -100 mV.(ABSTRACT TRUNCATED AT 400 WORDS)

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