scholarly journals The electrogenic Na+/HCO3−cotransport modulates resting membrane potential and action potential duration in cat ventricular myocytes

2007 ◽  
Vol 578 (3) ◽  
pp. 819-829 ◽  
Author(s):  
María C. Villa-Abrille ◽  
Martín G. Vila Petroff ◽  
Ernesto A. Aiello
Keyword(s):  
Membrane Potential ◽  
Action Potential ◽  
Action Potential Duration ◽  
Ventricular Myocytes ◽  
Resting Membrane Potential

scholarly journals Chloride current in mammalian cardiac myocytes. Novel mechanism for autonomic regulation of action potential duration and resting membrane potential.

1990 ◽  
Vol 95 (6) ◽  
pp. 1077-1102 ◽  
Author(s):  
R D Harvey ◽  
C D Clark ◽  
J R Hume
Keyword(s):  
Membrane Potential ◽  
Action Potential ◽  
Cardiac Myocytes ◽  
Action Potential Duration ◽  
Ventricular Myocytes ◽  
Reversal Potential ◽  
Chloride Current ◽  
Equilibrium Potential ◽  
Resting Membrane Potential ◽  
Dependent Pathway

The properties of the autonomically regulated chloride current (ICl) were studied in isolated guinea pig ventricular myocytes. This current was elicited upon exposure to isoproterenol (ISO) and reversed upon concurrent exposure to acetylcholine (ACh). ICl was time independent and exhibited outward rectification. The responses to ISO and ACh could be blocked by propranolol and atropine, respectively, and ICl was also elicited by forskolin, 8-bromoadenosine 3',5'-cyclic monophosphate, and 3-isobutyl-l-methylxanthine, indicating that the current is regulated through a cAMP-dependent pathway. The reversal potential of the ISO-induced current followed the predicted chloride equilibrium potential, consistent with it being carried predominantly by Cl-. Activation of ICl produced changes in the resting membrane potential and action potential duration, which were Cl- gradient dependent. These results indicate that under physiological conditions ICl may play an important role in regulating action potential duration and resting membrane potential in mammalian cardiac myocytes.

Modulation of membrane potential by an acetylcholine-activated potassium current in trout atrial myocytes

2007 ◽  
Vol 292 (1) ◽  
pp. R388-R395 ◽  
Author(s):  
Cristina E. Molina ◽  
Hans Gesser ◽  
Anna Llach ◽  
Lluis Tort ◽  
Leif Hove-Madsen
Keyword(s):  
Membrane Potential ◽  
Action Potential ◽  
Ventricular Myocytes ◽  
Reversal Potential ◽  
Membrane Potentials ◽  
Resting Membrane Potential ◽  
Atrial Myocytes ◽  
Atrial Tissue ◽  
Isolated Cardiac Myocytes ◽  
Inwardly Rectifying

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.

Distinct Membrane Effects of Spinal Nerve Ligation on Injured and Adjacent Dorsal Root Ganglion Neurons in Rats

2005 ◽  
Vol 103 (2) ◽  
pp. 360-376 ◽  
Author(s):  
Damir Sapunar ◽  
Marko Ljubkovic ◽  
Philipp Lirk ◽  
J Bruce McCallum ◽  
Quinn H. Hogan
Keyword(s):  
Membrane Potential ◽  
Dorsal Root Ganglion ◽  
Action Potential ◽  
Action Potential Duration ◽  
Dorsal Root ◽  
Spinal Nerve ◽  
Spinal Nerve Ligation ◽  
Dorsal Root Ganglion Neurons ◽  
Resting Membrane Potential ◽  
Ganglion Neurons

Background Painful peripheral nerve injury results in disordered sensory neuron function that contributes to the pathogenesis of neuropathic pain. However, the relative roles of neurons with transected axons versus intact adjacent neurons have not been resolved. An essential first step is identification of electrophysiologic changes in these two neuronal populations after partial nerve damage. Methods Twenty days after spinal nerve ligation (SNL), intracellular recordings were obtained from axotomized fifth lumbar (L5) dorsal root ganglion neurons and adjacent, intact L4 neurons, as well as from control neurons and others subjected to sham-SNL surgery. Results Pronounced electrophysiologic changes were seen only in L5 neurons after SNL. Both Aalpha/beta and Adelta neuron types showed increased action potential duration, decreased afterhyperpolarization amplitude and duration, and decreased current threshold for action potential initiation. Aalpha/beta neurons showed resting membrane potential depolarization, and increased repetitive firing during sustained depolarization developed in Adelta neurons. The afterhyperpolarization duration in neurons with C fibers shortened after axotomy. In contrast to the axotomized L5 neurons, neighboring L4 neurons showed no changes in action potential duration, afterhyperpolarization dimensions, or excitability after SNL. Depolarization rate (dV/dt) increased after SNL in L4 Aalpha/beta and Adelta neurons but decreased in L5 neurons. Time-dependent rectification during hyperpolarizing current injection (sag) was greater after SNL in Aalpha/beta L4 neurons compared with L5. Sham-SNL surgery produced only a decreased input resistance in Aalpha/beta neurons and a decreased conduction velocity in medium-sized cells. In the L5 ganglion after axotomy, a novel set of neurons, consisting of 24% of the myelinated population, exhibited long action potential durations despite myelinated neuron conduction velocities, particularly depolarized resting membrane potential, low depolarization rate, and absence of sag. Conclusions These findings indicate that nerve injury-induced electrical instability is restricted to axotomized neurons and is absent in adjacent intact neurons.

Effect of norepinephrine on Na(+)-K+ pump and Na+ influx in sheep cardiac Purkinje fibers

1990 ◽  
Vol 258 (4) ◽  
pp. C713-C722 ◽  
Author(s):  
S. W. Chae ◽  
D. Y. Wang ◽  
Q. Y. Gong ◽  
C. O. Lee
Keyword(s):  
Steady State ◽  
Membrane Potential ◽  
Action Potential ◽  
Action Potential Duration ◽  
Relative Magnitude ◽  
Resting Membrane Potential ◽  
Pacemaker Current ◽  
Purkinje Fibers ◽  
Cardiac Purkinje Fibers ◽  
High K

Effects of norepinephrine and Ca+ on Na(+)-K+ pump and pacemaker current were investigated by simultaneous measurement of intracellular Na+ activity (aiNa) and membrane potential in driven (1 Hz) and quiescent sheep cardiac Purkinje fibers. Concurrently, twitch force was measured in driven fibers, in which norepinephrine (NE) produced a decrease in aiNa, a prolongation in action potential duration, and a hyperpolarization in diastolic membrane potential, Vdm. In contrast, in quiescent fibers, NE produced an increase in aiNa and a depolarization in resting membrane potential, Vm. The decrease in aiNa, prolongation in action potential duration, and hyperpolarization in Vdm produced by NE were blocked by 5 x 10(-6) M strophanthidin, presumably through inhibition of the Na(+)-K+ pump. The increase in aiNa and membrane depolarization caused by NE were abolished by high [K+]o or Cs+, presumably through inhibition of the pacemaker current, if. These results indicate that in driven fibers NE stimulates predominantly the Na(+)-K+ pump, producing a decrease in aiNa and that in quiescent fibers it increases predominantly if, producing an increase in aiNa. The effect of NE on driven and quiescent fibers differs because of the voltage dependence of if and perhaps the Na(+)-K+ pump. Consequently, the relative magnitude of the two opposing effects of NE on aiNa appears to be dependent on membrane potential. In quiescent fibers, Cs+ monotonically decreased aiNa to a steady-state value, while Cs+ hyperpolarized membrane potential and then slowly depolarized to a steady-state level, producing a transient hyperpolarization. In driven fibers, Cs+ decreased aiNa, shortened action potential duration, and depolarized Vdm. Cs+ decreased aiNa more in quiescent fibers than in driven fibers. The decrease in aiNa and hyperpolarization in membrane potential produced by Cs+ in quiescent fibers were abolished by depolarization induced by high K+ extracellular concentration (25.4 mM) but were not abolished or reduced by 5 x 10(-6) M strophanthidin. These results suggest that the decrease in aiNa and hyperpolarization in membrane potential by Cs+ are caused by blockage of if but not by stimulation of the Na(+)-K+ pump and that if is an important source of Na+ loading into cells.

Electrophysiological response of rat ventricular myocytes to acidosis

2002 ◽  
Vol 283 (1) ◽  
pp. H412-H422 ◽  
Author(s):  
Kimiaki Komukai ◽  
Fabien Brette ◽  
Caroline Pascarel ◽  
Clive H. Orchard
Keyword(s):  
Membrane Potential ◽  
Action Potential ◽  
Ventricular Myocytes ◽  
Resting Potential ◽  
Disulfonic Acid ◽  
Resting Membrane Potential ◽  
Delayed Rectifier ◽  
Patch Clamp Technique ◽  
Electrophysiological Response ◽  
Inwardly Rectifying

The effects of acidosis on the action potential, resting potential, L-type Ca2+( I Ca), inward rectifier potassium ( I K1), delayed rectifier potassium ( I K), steady-state ( I SS), and inwardly rectifying chloride ( I Cl,ir) currents of rat subepicardial (Epi) and subendocardial (Endo) ventricular myocytes were investigated using the patch-clamp technique. Action potential duration was shorter in Epi than in Endo cells. Acidosis (extracellular pH decreased from 7.4 to 6.5) depolarized the resting membrane potential and prolonged the time for 50% repolarization of the action potential in Epi and Endo cells, although the prolongation was larger in Endo cells. At control pH, I Ca, I K1, and I SS were not significantly different in Epi and Endo cells, but I K was larger in Epi cells. Acidosis did not alter I Ca, I K1, or I K but decreased I SS; this decrease was larger in Endo cells. It is suggested that the acidosis-induced decrease in I SS underlies the prolongation of the action potential. I Cl,ir at control pH was Cd2+ sensitive but 4,4′-disothiocyanato-stilbene-2,2′-disulfonic acid resistant. Acidosis increased I Cl,ir; it is suggested that the acidosis-induced increase in I Cl,ir underlies the depolarization of the resting membrane potential.

Suppressive effect of acetylcholine on action potentials of canine paranodal fibers

1986 ◽  
Vol 251 (4) ◽  
pp. H710-H715
Author(s):  
W. W. Tse
Keyword(s):  
Membrane Potential ◽  
Action Potential ◽  
Action Potential Duration ◽  
Action Potentials ◽  
Conduction Block ◽  
Suppressive Effect ◽  
Resting Membrane Potential ◽  
Av Conduction ◽  
Av Conduction Block

The canine atrioventricular (AV) junction comprises three major tissues: paranodal fibers (PNF), AV node (AVN), and His bundle (HB). In the present study, dissection-exposed, in vitro canine AV junctional preparations were used. The object of the study was to determine whether the PNF or AVN was more sensitive to the suppressive effect of acetylcholine (ACh). In five experiments these tissues were stimulated antegradely and retrogradely, and their action potentials were recorded simultaneously under the influence of ACh (0.5 micrograms/ml). Results indicated the PNF were more sensitive to the suppressive effect of ACh than were the AVN. In another group of 13 experiments, the effects of ACh at 0.05-0.3 micrograms/ml on rate of rise of phase 0 of action potentials (Vmax), peak potential, resting membrane potential, and action potential duration of the PNF were determined. Results indicated that ACh exerted a strong suppressive effect on Vmax and amplitude of the action potentials and had little effect on the resting membrane potential and action potential duration of the PNF. In 10 of 13 preparations, ACh also suppressed the response of PNF, resulting in generation of one action potential to every two stimuli. In conclusion, these findings suggest that PNF could be the tissue responsible for vagal-induced AV conduction block.

Contribution of a swelling-activated chloride current to changes in the cardiac action potential

1997 ◽  
Vol 273 (2) ◽  
pp. C541-C547 ◽  
Author(s):  
J. I. Vandenberg ◽  
G. C. Bett ◽  
T. Powell
Keyword(s):  
Membrane Potential ◽  
Action Potential ◽  
Action Potentials ◽  
Ventricular Myocytes ◽  
Cell Swelling ◽  
Disulfonic Acid ◽  
Resting Membrane Potential ◽  
Cardiac Action ◽  
Cell Recording ◽  
Induced Changes

The purpose of this investigation was to determine to what extent the swelling-activated Cl- current (ICl,swell) contributes to swelling-induced changes in the resting membrane potential and action potential duration (APD) in ventricular myocytes. Action potentials were recorded from guinea pig ventricular myocytes using conventional whole cell recording techniques. Cell swelling caused initial lengthening followed by a variable shortening of APD. In 59% of cells this secondary APD shortening had a 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS)-sensitive component, consistent with a contribution from ICl,swell. Furthermore, DIDS partially antagonized the depolarization of the resting membrane potential that occurred during cell swelling. We have modeled the ICl,swell using the Oxsoft Heart computer program. Action potential changes predicted by the model agree well with the observed DIDS-sensitive component of the change in the action potential during cell swelling. We conclude that activation of ICl,swell contributes to shortening of APD and depolarization of the resting membrane potential during cell swelling in cardiac myocytes.

Chloride conductance pathways in heart

1991 ◽  
Vol 261 (3) ◽  
pp. C399-C412 ◽  
Author(s):  
J. R. Hume ◽  
R. D. Harvey
Keyword(s):  
Membrane Potential ◽  
Action Potential ◽  
Cardiac Muscle ◽  
Action Potential Duration ◽  
Historical Perspective ◽  
Outward Current ◽  
Resting Membrane Potential ◽  
Transient Outward Current ◽  
K Current ◽  
Cl Conductance

Nonelectrogenic movement of Cl- is believed to be responsible for the active accumulation of intracellular Cl- in cardiac muscle. The electro-neutral pathways underlying this nonpassive distribution of Cl- are believed to include Cl(-)-HCO3- exchange, Na(+)-dependent cotransport (operating as Na(+)-Cl- and Na(+)-K(+)-2Cl- cotransport), and K(+)-Cl- cotransport. The electrogenic movement of Cl- in cardiac muscle is particularly interesting from a historical perspective. Until recently, there was some doubt as to whether Cl- carried any current in the heart. Early microelectrode experiments indicated that a Cl- conductance probably played an important role in regulating action potential duration and resting membrane potential. Subsequent voltage-clamp experiments identified a repolarizing, transient outward current that was believed to be conducted by Cl-, yet further investigation suggested that this transient outward current was more likely a K+ current, not a Cl- current. This left some doubt as to whether Cl- played any role in regulating membrane potential in cardiac muscle. More recent studies, however, have identified a highly selective Cl- conductance that is regulated by intracellular adenosine 3',5'-cyclic monophosphate, and it appears that this Cl- current may play an important role in the regulation of action potential duration and resting membrane potential.

Dual effects of external magnesium on action potential duration in guinea pig ventricular myocytes

1995 ◽  
Vol 268 (6) ◽  
pp. H2321-H2328 ◽  
Author(s):  
S. Zhang ◽  
T. Sawanobori ◽  
H. Adaniya ◽  
Y. Hirano ◽  
M. Hiraoka
Keyword(s):  
Guinea Pig ◽  
Action Potential ◽  
Decay Time ◽  
Action Potential Duration ◽  
Time Course ◽  
Ventricular Myocytes ◽  
Membrane Surface ◽  
Surface Charges ◽  
Whole Cell Patch Clamp ◽  
K Current

Effects of extracellular magnesium (Mg2+) on action potential duration (APD) and underlying membrane currents in guinea pig ventricular myocytes were studied by using the whole cell patch-clamp method. Increasing external Mg2+ concentration [Mg2+]o) from 0.5 to 3 mM produced a prolongation of APD at 90% repolarization (APD90), whereas 5 and 10 mM Mg2+ shortened it. [Mg2+]o, at 3 mM or higher, suppressed the delayed outward K+ current and the inward rectifier K+ current. Increases in [Mg2+]o depressed the peak amplitude and delayed the decay time course of the Ca2+ current (ICa), the latter effect is probably due to the decrease in Ca(2+)-induced inactivation. Thus 3 mM Mg2+ suppressed the peak ICa but increased the late ICa amplitude at the end of a 200-ms depolarization pulse, whereas 10 mM Mg2+ suppressed both components. Application of 10 mM Mg2+ shifted the voltage-dependent activation and inactivation by approximately 10 mV to more positive voltage due to screening the membrane surface charges. Application of manganese (1-5 mM) also caused dual effects on APD90, similar to those of Mg2+, and suppressed the peak ICa with slowed decay. These results suggest that the dual effects of Mg2+ on APD in guinea pig ventricular myocytes can be, at least in part, explained by its action on ICa with slowed decay time course in addition to suppressive effects on K+ currents.

scholarly journals Phenanthrene impacts zebrafish cardiomyocyte excitability by inhibiting IKr and shortening action potential duration

2021 ◽  
Vol 153 (2) ◽  
Author(s):  
Shiva N. Kompella ◽  
Fabien Brette ◽  
Jules C. Hancox ◽  
Holly A. Shiels
Keyword(s):  
Air Pollution ◽  
Action Potential ◽  
Action Potential Duration ◽  
Cardiac Electrophysiology ◽  
Resting Membrane Potential ◽  
Dependent Manner ◽  
Polyaromatic Hydrocarbon ◽  
Premature Ventricular Contractions ◽  
Whole Cell Patch Clamp ◽  
Dose Dependent

Air pollution is an environmental hazard that is associated with cardiovascular dysfunction. Phenanthrene is a three-ringed polyaromatic hydrocarbon that is a significant component of air pollution and crude oil and has been shown to cause cardiac dysfunction in marine fishes. We investigated the cardiotoxic effects of phenanthrene in zebrafish (Danio rerio), an animal model relevant to human cardiac electrophysiology, using whole-cell patch-clamp of ventricular cardiomyocytes. First, we show that phenanthrene significantly shortened action potential duration without altering resting membrane potential or upstroke velocity (dV/dt). L-type Ca2+ current was significantly decreased by phenanthrene, consistent with the decrease in action potential duration. Phenanthrene blocked the hERG orthologue (zfERG) native current, IKr, and accelerated IKr deactivation kinetics in a dose-dependent manner. Furthermore, we show that phenanthrene significantly inhibits the protective IKr current envelope, elicited by a paired ventricular AP-like command waveform protocol. Phenanthrene had no effect on other IK. These findings demonstrate that exposure to phenanthrene shortens action potential duration, which may reduce refractoriness and increase susceptibility to certain arrhythmia triggers, such as premature ventricular contractions. These data also reveal a previously unrecognized mechanism of polyaromatic hydrocarbon cardiotoxicity on zfERG by accelerating deactivation and decreasing IKr protective current.

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