Fluid Pressure Triggers Action Potential and a Subsequent Transverse Ca2+ Wave via Na+‒CA2+ Exchange Activated by Insp3 Receptor-Mediated Local Ca2+ Wave in Rat Atrial Myocytes

Application of the current-clamp technique in rainbow trout atrial myocytes has yielded resting membrane potentials that are incompatible with normal atrial function. To investigate this paradox, we recorded the whole membrane current ( Im) and compared membrane potentials recorded in isolated cardiac myocytes and multicellular preparations. Atrial tissue and ventricular myocytes had stable resting potentials of −87 ± 2 mV and −83.9 ± 0.4 mV, respectively. In contrast, 50 out of 59 atrial myocytes had unstable depolarized membrane potentials that were sensitive to the holding current. We hypothesized that this is at least partly due to a small slope conductance of Im around the resting membrane potential in atrial myocytes. In accordance with this hypothesis, the slope conductance of Im was about sevenfold smaller in atrial than in ventricular myocytes. Interestingly, ACh increased Im at −120 mV from 4.3 pA/pF to 27 pA/pF with an EC50 of 45 nM in atrial myocytes. Moreover, 3 nM ACh increased the slope conductance of Im fourfold, shifted its reversal potential from −78 ± 3 to −84 ± 3 mV, and stabilized the resting membrane potential at −92 ± 4 mV. ACh also shortened the action potential in both atrial myocytes and tissue, and this effect was antagonized by atropine. When applied alone, atropine prolonged the action potential in atrial tissue but had no effect on membrane potential, action potential, or Im in isolated atrial myocytes. This suggests that ACh-mediated activation of an inwardly rectifying K+ current can modulate the membrane potential in the trout atrial myocytes and stabilize the resting membrane potential.

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Impact of Sarcoplasmic Reticulum Calcium Release on Calcium Dynamics and Action Potential Morphology in Human Atrial Myocytes: A Computational Study

PLoS Computational Biology ◽

10.1371/journal.pcbi.1001067 ◽

2011 ◽

Vol 7 (1) ◽

pp. e1001067 ◽

Cited By ~ 67

Author(s):

Jussi T. Koivumäki ◽

Topi Korhonen ◽

Pasi Tavi

Keyword(s):

Sarcoplasmic Reticulum ◽

Action Potential ◽

Calcium Release ◽

Computational Study ◽

Calcium Dynamics ◽

Atrial Myocytes ◽

Human Atrial Myocytes ◽

Sarcoplasmic Reticulum Calcium

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Fluid Pressure-Activated Non-Selective Cation Current and Cl- Current in Rat Atrial Myocytes

Biophysical Journal ◽

10.1016/j.bpj.2012.11.1589 ◽

2013 ◽

Vol 104 (2) ◽

pp. 284a

Author(s):

Min-Jeong Son ◽

Sun-Hee Woo

Keyword(s):

Fluid Pressure ◽

Atrial Myocytes ◽

Cation Current

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Calcitonin gene-related peptide increases Ca2+ and K+ currents and prolongs the action potential duration in guinea pig atrial myocytes.

The Japanese Journal of Pharmacology ◽

10.1016/s0021-5198(19)39498-3 ◽

1991 ◽

Vol 55 ◽

pp. 370

Author(s):

Kageyoshi Ono ◽

Wayne R. Giles

Keyword(s):

Guinea Pig ◽

Action Potential ◽

Action Potential Duration ◽

Calcitonin Gene Related Peptide ◽

Atrial Myocytes ◽

Related Peptide ◽

Calcitonin Gene ◽

K Currents

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

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1997.272.1.h227 ◽

1997 ◽

Vol 272 (1) ◽

pp. H227-H235 ◽

Cited By ~ 18

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.

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

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1997.272.4.h1798 ◽

1997 ◽

Vol 272 (4) ◽

pp. H1798-H1803 ◽

Cited By ~ 4

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.

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Role of chloride currents in repolarizing rabbit atrial myocytes

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1995.268.5.h1992 ◽

1995 ◽

Vol 268 (5) ◽

pp. H1992-H2002 ◽

Cited By ~ 4

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.

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Contribution of Na+/Ca2+ exchange to action potential of human atrial myocytes

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1996.271.3.h1151 ◽

1996 ◽

Vol 271 (3) ◽

pp. H1151-H1161 ◽

Cited By ~ 12

Author(s):

A. Benardeau ◽

S. N. Hatem ◽

C. Rucker-Martin ◽

B. Le Grand ◽

L. Mace ◽

...

Keyword(s):

Action Potential ◽

Action Potentials ◽

Time Course ◽

Significant Proportion ◽

Type A ◽

Plateau Phase ◽

Type B ◽

Atrial Myocytes ◽

Human Atrial Myocytes ◽

Delayed Afterdepolarizations

The Ca2+ dye indo 1 was used to record internal Ca2+ (Cai) transients in order to investigate the role of the Na+/Ca2+ exchange current (INa/Ca) in whole cell patch-clamped human atrial myocytes After the activation of the L-type Ca2+ current by test pulses (20 ms) at +20 mV, a tail current (I(tail)) was activated at a holding potential of -80 mV with a density of -1.29 +/- 0.06 pA/pF. The time course of I(tail) followed that of Cai transients I(tail) was suppressed by dialyzing cells with ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid, applying 5 mM caffeine, or substituting external Na+ with Li+, indicating that this current was mainly generated by INa/Ca. Two types of action potential were recorded: type A, which is characterized by a narrow early plateau followed by a late low plateau phase, and type B, which is characterized by a small initial peak followed by a prolonged high plateau phase. Type B action potentials were found in larger cells than type A action potentials (membrane capacitance 81.8 +/- 4.5 and 122.4 +/- 7.0 pF in types A and B, respectively, P < 0.001). Substitution of external Na+ with Li+ shortened the late plateau of the type A action potential and the prolonged plateau of the type B action potential. Suppression of Cai transients by caffeine shortens the late part of both types of action potentials, whereas its lengthening effect on the initial phase of action potentials can result from several different mechanisms. The beat-to-beat dependent relationship between Cai transients and action potentials could be mediated by Ina/Ca- Delayed afterdepolarizations were present in a significant proportion of atrial myocytes in our experimental conditions. They were reversibly suppressed by Li+ substitution for Na+, suggesting that they are generated by INa/Ca. We conclude that INa/Ca plays a major role in the development of action potentials and delayed afterdepolarizations in isolated human atrial myocytes.

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