scholarly journals A Mathematical Model of Action Potential in the Rat Atrial Cells

2019 ◽  
Author(s):  
Na Zhao ◽  
Yimei Du ◽  
Kuanquan Wang ◽  
Henggui Zhang ◽  
Qince Li
Keyword(s):  
Mathematical Model ◽  
Action Potential ◽  
Atrial Cells ◽  
Rat Atrial Cells

Cl - channels in Chara

1982 ◽  
Vol 299 (1097) ◽  
pp. 435-445 ◽  
Keyword(s):  
Mathematical Model ◽  
Action Potential ◽  
Voltage Dependence ◽  
Quantitative Description ◽  
Chara Corallina ◽  
Squid Axon ◽  
Impedance Measurements ◽  
Time Constants ◽  
Effects Of Ph ◽  
Cl Channels

The action potential in the cells of the freshwater alga Chara corallina is slower than that in the nerve by about 1000-fold. The depolarization phase is brought on by the outflow of the Cl - ions. Voltage-clamp studies show that this Cl - current can be described by the Hodgkin-Huxley equations for the Na+ transient in the squid axon. The only change necessary to the form of the Hodgkin-Huxley equations is an introduction of a time delay between the stimulus and the onset of excitation. This mathematical model of the Chara action potential facilitates a quantitative description of the effects of pH and temperature. While a pH shift alters various Hodgkin-Huxley parameters, temperature change influences mainly the activation and inactivation time constants but leaves the voltage-dependence of these parameters unaffected. The delays in excitation are both temperature and potential dependent. In future some corrections to the Hodgkin-Huxley picture of the Chara action potential may be necessary, as recent impedance measurements suggest a change in the membrane capacitance at the time of excitation.

Properties of human atrial ICa at physiological temperatures and relevance to action potential

1997 ◽  
Vol 272 (1) ◽  
pp. H227-H235 ◽  
Author(s):  
G. R. Li ◽  
S. Nattel
Keyword(s):  
Action Potential ◽  
Human Atrium ◽  
Atrial Myocytes ◽  
Human Atrial Myocytes ◽  
Maximum Current Density ◽  
Rate Dependent ◽  
Atrial Cells ◽  
Maximum Current ◽  
Reduced Rate

There are no published characterizations of Ca2+ current (ICa) at physiological temperatures in human atrium. Depolarization of human atrial myocytes at 36 degrees C elicited ICa that peaked at +10 mV, with a mean maximum current density of 10.8 +/- 1.1 pA/pF and no evidence for T-type current. Overlap between activation and inactivation curves and incomplete inactivation during pulses comparable to normal action potential duration (APD) were compatible with the observed role of ICa in maintaining the plateau. ICa was frequency dependent between 0.1 and 2 Hz and ICa blockade with 0.2 mM Cd2+ reduced rate-dependent changes in APD: under control, APD at 90% repolarization was 230 +/- 15 ms at 0.1 Hz and 178 +/- 14 ms at 2 Hz (decrease of 52 +/- 5 ms); with Cd2+, values were 121 +/- 7 ms at 0.1 H2 and 115 +/- 6 ms at 2 Hz (decrease of 6 +/- 3 ms, P < 0.01) Isoproterenol (1 microM) increased ICa and prolonged APD from 138 +/- 13 to 199 +/- 15 ms (P < 0.01). These results indicate that, in human atrial cells at 36 degrees C, the properties of L-type ICa contribute importantly to the rate-dependent and autonomic control of APD.

Effects of relaxin on rat atrial myocytes. II. Increased calcium influx derived from action potential prolongation

1997 ◽  
Vol 272 (4) ◽  
pp. H1798-H1803 ◽  
Author(s):  
E. S. Piedras-Renteria ◽  
O. D. Sherwood ◽  
P. M. Best
Keyword(s):  
Action Potential ◽  
Calcium Influx ◽  
Calcium Currents ◽  
Atrial Myocytes ◽  
Inotropic Effects ◽  
Whole Cell Patch Clamp ◽  
Rat Hearts ◽  
Action Potential Prolongation ◽  
Dose Dependent ◽  
Rat Atrial Cells

Relaxin produces positive inotropic and chronotropic effects in rat hearts. The effect of relaxin on the action potential duration (APD) of single quiescent rat atrial cells was investigated with a whole cell patch clamp. Relaxin induced a significant, dose-dependent prolongation of the APD. This effect was maximal at 200 ng/ml (nominal concentration of 33.6 nM), which caused, on average, a 57% increase in the time taken to reach 90% repolarization. The effect of relaxin was blocked by the protein kinase A inhibitor 5-24 amide, indicating that its effect is mediated by an adenosine 3',5'-cyclic monophosphate-dependent mechanism. The increased APD induced by relaxin caused an enhanced entrance of calcium, with the charge carried through voltage-activated calcium channels increased by approximately 25%. This increase was not due to a direct modulation of calcium currents (20); rather, it was a consequence of the longer period of cellular depolarization. Our findings that relaxin increased the APD and therefore increased the calcium influx in atrial myocytes could explain the positive inotropic effects induced by relaxin in atrial preparations.

Determinants of action potential initiation in isolated rabbit atrial and ventricular myocytes

1998 ◽  
Vol 274 (6) ◽  
pp. H1902-H1913 ◽  
Author(s):  
David A. Golod ◽  
Rajiv Kumar ◽  
Ronald W. Joyner
Keyword(s):  
Action Potential ◽  
Ventricular Myocytes ◽  
Cell Types ◽  
Membrane Properties ◽  
Resting Membrane Potential ◽  
Isolated Cells ◽  
Atrial Cells ◽  
Ventricular Cells ◽  
Action Potential Initiation ◽  
Potential Initiation

Action potential conduction through the atrium and the ventricle of the heart depends on the membrane properties of the atrial and ventricular cells, particularly with respect to the determinants of the initiation of action potentials in each cell type. We have utilized both current- and voltage-clamp techniques on isolated cells to examine biophysical properties of the two cell types at physiological temperature. The resting membrane potential, action potential amplitude, current threshold, voltage threshold, and maximum rate of rise measured from atrial cells (−80 ± 1 mV, 109 ± 3 mV, 0.69 ± 0.05 nA, −59 ± 1 mV, and 206 ± 17 V/s, respectively; means ± SE) differed significantly ( P < 0.05) from those values measured from ventricular cells (−82.7 ± 0.4 mV, 127 ± 1 mV, 2.45 ± 0.13 nA, −46 ± 2 mV, and 395 ± 21 V/s, respectively). Input impedance, capacitance, time constant, and critical depolarization for activation also were significantly different between atrial (341 ± 41 MΩ, 70 ± 4 pF, 23.8 ± 2.3 ms, and 19 ± 1 mV, respectively) and ventricular (16.5 ± 5.4 MΩ, 99 ± 4.3 pF, 1.56 ± 0.32 ms, and 36 ± 1 mV, respectively) cells. The major mechanism of these differences is the much greater magnitude of the inward rectifying potassium current in ventricular cells compared with that in atrial cells, with an additional difference of an apparently lower availability of inward Na current in atrial cells. These differences in the two cell types may be important in allowing the atrial cells to be driven successfully by normal regions of automaticity (e.g., the sinoatrial node), whereas ventricular cells would suppress action potential initiation from a region of automaticity (e.g., an ectopic focus).

Role of chloride currents in repolarizing rabbit atrial myocytes

1995 ◽  
Vol 268 (5) ◽  
pp. H1992-H2002 ◽  
Author(s):  
Z. Wang ◽  
B. Fermini ◽  
J. Feng ◽  
S. Nattel
Keyword(s):  
Action Potential ◽  
Reversal Potential ◽  
Outward Current ◽  
Cell Voltage ◽  
Disulfonic Acid ◽  
Transient Outward Current ◽  
Atrial Myocytes ◽  
Atrial Cells ◽  
K Current

Rabbit atrial cells manifest a prominent transient outward K+ current (Ito1), but this current recovers slowly from inactivation and is unlikely to be important at physiological rates (3-5 Hz). Depolarization of rabbit atrial cells also elicits a transient Ca(2+)-dependent outward Cl- current (Ito2). To compare the relative magnitude of these transient outward currents at various rates, we applied whole cell voltage-clamp techniques to isolated rabbit atrial myocytes. Whereas peak Ito1 exceeded Ito2 at slow rates (0.1 Hz), Ito1 was strongly reduced as rate was increased (by 97 +/- 2%, mean +/- SE, at 4 Hz), while Ito2 was slightly reduced (by 28 +/- 4%, 4 Hz). The reversal potential of transient outward tail currents at 0.07 Hz was -49 +/- 9 mV, while at 2.5 Hz the reversal potential became -18 +/- 7 mV (calculated Cl- reversal potential -18 mV). The addition of the Cl- transport blocker 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS; 150 microM) or the replacement of external Cl- with methanesulfonate inhibited a large part of the transient outward current elicited by depolarization at 4 Hz. DIDS and Cl- replacement increased action potential duration in both single rabbit atrial cells and multicellular rabbit atrial preparations. We conclude that the Ca(2+)-dependent Cl- current is substantially larger than the transient K+ current at physiological rates in the rabbit and is likely to play a more important role in action potential repolarization than the latter current in this tissue in vivo.

Mathematical model of the ventricular action potential and effects of isoproterenol-induced cardiac hypertrophy in rats

2020 ◽  
Vol 49 (5) ◽  
pp. 323-342
Author(s):  
Sevgi Şengül Ayan ◽  
Ahmet K. Sırcan ◽  
Mohamedou Abewa ◽  
Ahmet Kurt ◽  
Uğur Dalaman ◽  
...  
Keyword(s):  
Mathematical Model ◽  
Action Potential ◽  
Cardiac Hypertrophy ◽  
Ventricular Action Potential
Sign in / Sign up

Export Citation Format

Share Document