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PubMed1985

Effects of selective channel blocking agents on contractions and action potentials in K+-depolarized guinea-pig atria.

Contractions and transmembrane action potentials were induced by 1 microM isoprenaline in K+-depolarized guinea-pig left atria driven at 0.5 Hz. The stability of these responses was significantly increased by doubling the extracellular glucose concentration to 22 mM. Action potential overshoot increased by 28 mV per ten fold increase in extracellular calcium concentration suggesting that the inward current in this preparation is carried by Ca2+. In depolarized driven preparations, nanomolar concentrations of nifedipine and nisoldipine reduced contractility, maximum rate of depolarization (dV/dt max) and action potential height, whereas the fast channel blocking agents tetrodotoxin and mexiletine (in micromolar concentrations) produced little change. Nifedipine also rendered spontaneously beating depolarized right atrial preparations quiescent. In concentrations which reduced dV/dt of normal action potentials, the sodium channel blocking agents quinidine and Org 6001 reduced the amplitude of contractions and reduced the maximum rate of phase 0 depolarization (dV/dt) of action potentials in depolarized tissue. These actions were reversed by Ca2+ and suggest calcium antagonistic activity. However action potential height was not reduced. Like bepridil, both drugs also reduced the frequency of spontaneous contractions in depolarized right atrial preparations. Unlike Org 6001, quinidine failed to produce a shift in calcium log dose-response curves in driven depolarized preparations and induced positive inotropy in the presence of functional sodium channels. Bepridil inhibited contractions in depolarized atria in the absence of a reduction in dV/dt suggesting that any calcium antagonistic action in atrial tissue is mainly located at an intracellular site. In conclusion, action potentials elicited by isoprenaline in potassium-depolarized atria bathed in high glucose appear to be Ca2+ mediated. In concentrations which inhibit the inward Na+ current, both quinidine and Org 6001 exhibit calcium channel blocking properties.

Action Potentials↗

PubMed1982

Is action potential duration of the intact dog heart related to contractility or stimulus rate?

1. The contractility (maximum rate of rise of left ventricular pressure) and action potential duration were measured in intact closed-chest anaesthetized dogs with complete atrioventricular dissociation and beta-adrenergic blockade.2. Measurements were confined to test beats following a 1 sec interval. Prior to the test interval (priming period) a variety of potentiating stimulus trains were introduced.3. When the frequency of stimulation was increased in the priming period (frequency potentiation), there was an inverse relationship between action potential duration and contractility of the test beat.4. When the test beat was potentiated by a single beat terminating the priming period with one short interval (post-extrasystolic potentiation), there was no relationship between the action potential duration and contractility of the test beat.5. Paired pulse stimulation was used for any given frequency to vary contractility by short interval potentiation. For any given frequency of stimulation there was no relationship between action potential duration and contractility of the test beat. For any given value of contractility, action potential duration decreased with increased frequency of stimulation.6. The introduction of a high frequency train caused a step decrease in action potential duration on the first beat of the train. This was followed by a further slow decline in action potential duration with a time course of over 3 min. These two changes could be dissociated by the introduction during the train of one second interval test pulses, which only showed the slow shortening.7. The lack of a consistent relationship between action potential duration and contractility of the test beat disagrees with the hypothesis that repolarization is controlled by the activator calcium responsible for the contractility. The action potential shortening associated with increased frequency is related to the frequency change per se.8. The slow time course of change in action potential duration following an increase in stimulation frequency suggests that these changes are caused by the accumulation of an ion or metabolite, or possibly by changes of activity of the electrogenic Na(+)-K(+) pump.

Action Potentials↗

PubMed1987

Action potential fatigue in single skeletal muscle fibres of Xenopus.

Action potential fatigue has been studied in single short toe muscle fibres of Xenopus under three different conditions: in rested fibres which produced maximum tension, in fibres during post-contractile depression (PCD), a state of depressed tension generation but seemingly normal membrane properties, and in fibres de-tubulated by glycerol treatment. The fibres were stimulated continuously at 70 Hz (22.5 degrees C) and membrane potential was measured throughout the stimulation period with an intracellular microelectrode. Rested and PCD fibres exhibited similarities in the development of action potential fatigue during a 30 s stimulation period; the amplitude was reduced by 86 and 70 mV, respectively, and the duration, measured at a level of one-third of the peak amplitude, was increased from 1.1 to 4.2 and 1.3 to 3.7 ms, respectively. De-tubulated fibres were more resistant to action potential fatigue; the amplitude decreased by only 20 and 35 mV during 30 and 60 s of stimulation, respectively, and the duration was increased from 1.1 to 2.7 ms. It is concluded that action potential fatigue in skeletal muscle fibres is primarily caused by failing regenerative activity in the t-tubules, which is reflected in an altered shape of conventionally recorded action potentials.

Action Potentials↗

PubMed1982

Effects of Ca ions on action potentials in immature cultured neurons from chick cerebral cortex.

Action potentials evoked by depolarizing pulses were studied in immature cultured cerebral cortical neurons from chick embryos. The majority of action potentials were rather small, and they were still elicited in the presence of 10(-7) gm/ml tetrodotoxin (TTX), but were almost completely abolished in NA+-free solution or by 10(-5) gm/ml TTX in Tyrode's solution. The elevation of external Ca2+ concentration not only increased the maximum rates of rise of action potentials in normal Tyrode's solution with and without low (10(-7) gm/ml) TTX but also regenerated action potentials in high (10(-5) gm/ml) TTX-containing Tyrode's solution or in Na+-free solution. These high Ca2+ effects were blocked by Mn2+ or Co2+. These results suggest that action potentials, which were predominantly Na-dependent, are partially contributed by Ca ions in immature chick cerebral cortical neurons.

Action Potentials↗

PubMed1999

Contractile activity in intestinal muscle evokes action potential discharge in guinea-pig myenteric neurons.

1. The process by which stretch of the external muscle of the intestine leads to excitation of myenteric neurons was investigated by intracellular recording from neurons in isolated longitudinal muscle-myenteric plexus preparations from the guinea-pig. 2. Intestinal muscle that was stretched by 40 % beyond its resting size in either the longitudinal or circular direction contracted irregularly. Both multipolar, Dogiel type II, neurons and uniaxonal neurons generated action potentials in stretched tissue. Action potentials persisted when the membrane potential was hyperpolarized by passing current through the recording electrode for 10 of 14 Dogiel type II neurons and 1 of 18 uniaxonal neurons, indicating that the action potentials originated in the processes of these neurons. For the remaining four Dogiel type II and 17 uniaxonal neurons, the action potentials were abolished, suggesting that they were the result of synaptic activation of the cell bodies. 3. Neurons did not fire action potentials when the muscle was paralysed by nicardipine (3 microM), even when the preparations were simultaneously stretched by 50 % beyond resting length in longitudinal and circular directions. Spontaneous action potentials were not recorded in unstretched (slack) tissue, but when the L-type calcium channel agonist (-)-Bay K 8644 (1 microM) was added, the muscle contracted and action potentials were observed in Dogiel type II neurons and uniaxonal neurons. 4. The proteolytic enzyme dispase (1 mg ml-1) added to preparations that were stretched 40 % beyond slack width caused the myenteric plexus to lift away from the muscle, but did not prevent muscle contraction. In the presence of dispase, the neurons ceased firing action potentials spontaneously, although action potentials could still be evoked by intracellular current pulses. After the action of dispase, (-)-Bay K 8644 (1 microM) contracted the muscle but did not cause neurons to fire action potentials. 5. Gadolinium ions (1 microM), which block some stretch activated ion channels, stopped muscle contraction and prevented action potential firing in tissue stretched by 40 %. However, when (-)-Bay K 8644 (1 microM) was added in the presence of gadolinium, the muscle again contracted and action potentials were recorded from myenteric neurons. 6. Stretching the tissue 40 % beyond its slack width caused action potential firing in preparations that had been extrinsically denervated and in which time had been allowed for the cut axons to degenerate. 7. The present results lead to the following hypotheses. The neural response to stretching depends on the opening of stretch activated channels in the muscle, muscle contraction in response to this opening, and mechanical communication from the contracting muscle to myenteric neurons. Distortion of sensitive sites in the processes of the neurons opens channels to initiate action potentials that are propagated to the soma, where they are recorded. Neurons are also excited indirectly by slow synaptic transmission from neurons that respond directly to distortion.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗

PubMed1994

The origin of the effects of an anticholinesterase on the latencies of action potentials in mouse skeletal muscles.

1. Subcutaneous injection in mice of a single dose of an organophosphorous anticholinesterase, ecothiopate (0.5 mumol kg-1), produced increased variability in the latency (jitter) of indirectly-elicited action potentials in diaphragm muscles 5 days after treatment, but there was no effect on the variability of latencies of endplate potentials. This study was designed to elucidate the mechanism(s) of the increase in action potential jitter. 2. Action potentials evoked directly by electrical stimulation at one end of muscle fibres and recording near the other end had less jitter than indirectly-evoked action potentials and ecothiopate had no effect on directly-evoked action potentials. 3. In preparations with uncut fibres, pretreatment with ecothiopate reduced by about 20% both muscle fibre input resistance and the amplitude of spontaneous miniature endplate potentials. Ecothiopate had no effect on muscle fibre resting membrane potential or on the threshold potential for excitation. 4. In untreated preparations, indirectly-evoked action potentials recorded at the endplate had similar jitter to action potentials recorded at the tendon when latencies were measured at 10% of peak amplitude. However, when latencies were measured at peak, there was greater jitter of action potentials at the endplate. Ecothiopate increased jitter of action potentials recorded at the endplate at 10% of peak but did not significantly increase jitter of action potentials recorded at the endplate when measured at the peak. 5. In cut-fibre preparations, the first endplate potential of trains was significantly increased after ecothiopate but there was no effect of ecothiopate on the amplitude of plateau endplate potentials later in the train. Analysis of plateau endplate potentials showed that 5 days after administration, ecothiopateproduced an increase in the variance of endplate potential amplitudes and changes in the binomial parameters n and p.6. It was concluded that the increased jitter produced by ecothiopate is not a generalized effect on the plasma membrane and that none of the above observations could explain the increased jitter. The possibility is discussed that increased jitter is produced by variability in times to threshold of endplate potentials and/or by variability in the locus of generation of the action potential in the perijunctional area.

Action Potentials↗

PubMed2000

Dopamine D1 receptors synergize with D2, but not D3 or D4, receptors in the striatum without the involvement of action potentials.

The widespread biological actions of the neurotransmitter dopamine (DA) are mediated by two classes of receptor, the D(1) class (D(1) and D(5)) and the D(2) class (D(2), D(3), and D(4)), which interact synergistically in many paradigms, such as DA agonist-stimulated motor behavior and striatal c-fos expression. Understanding the mechanism(s) of this interaction has been impeded by a controversy regarding the cellular localization of D(1) and D(2) class receptors. To address this issue from a functional point of view, we elicited striatal Fos by combined administration of a D(1) class and a D(2) class agonist either in the presence or absence of the fast sodium channel blocker tetrodotoxin (TTX). Striatal Fos elicited by direct D(1)/D(2) stimulation was not reduced by TTX. By contrast, TTX greatly attenuated the Fos response evoked by cocaine or GBR 12909. In separate experiments using antagonists that distinguish among members of the D(2) class of receptors, amphetamine-stimulated Fos and motor behavior were attenuated dose-dependently by the selective D(2) antagonist L-741,626, but not by the selective D(3) antagonist U99194A or the D(4)-selective antagonist L-745,870. Because Fos expression in the paradigms that were used occurs in enkephalin-negative striatonigral neurons, which show limited coexpression of D(1) and D(2) receptors, the present findings taken together suggest the intriguing possibility that D(1)/D(2) synergism may be mediated by D(1) and D(2) receptors residing on separate striatal neurons and interacting in a manner that is not dependent on action potentials.

Action Potentials↗

PubMed1989

Calcium currents in single SA nodal cells of the rabbit heart studied with action potential clamp.

With a new method called "Action Potential-Clamp" (APC) we studied in single SA nodal cells the contribution of both transient and long lasting calcium currents (L-type and T-type) to the action potential. Action potentials were recorded by a computer and a representative cycle was subsequently repetitively replayed to the same cell under voltage clamp. Blockade of the L-type calcium current (D600) or T-type calcium current (nickel) revealed the quantitative and time related contributions of these currents to the action potential, since the blocked current is compensated by the clamp amplifier.

Action Potentials↗

PubMed2003

Streptozotocin-diabetes alters action potentials in rat diaphragm.

This study tested the hypothesis that diabetes alters diaphragm action potentials and electrophysiological responses to K(+) channel blockade. Intracellular recordings were performed in vitro in diaphragm fibers from streptozotocin-induced diabetic and normal Wistar rats (glucose 670+/-31 vs. 252+/-14 mg/dl). Comparing diabetic to normal muscle properties, resting membrane potential was significantly depolarized (-72.2+/-0.8 vs. -77.4+/-1.1 mV), action potential 50% repolarization time was significantly accelerated (0.33+/-0.01 vs. 0.39 +/-0.01 msec), and action potential area was significantly decreased (59.4+/-2.3 vs. 70.7+/-2.2 mV msec). The K(+) channel blocker 3,4-diaminopyridine (DAP) depolarized resting membrane potential of normal but not diabetic muscle. DAP significantly prolonged action potential repolarization and significantly increased action potential area, but significantly more in normal than diabetic muscle. These data indicate that diabetes shortens diaphragm action potentials, which appears to be due to altered K(+) channels.

4-Aminopyridine↗

PubMed1985

Effect of higenamine on action potential of Purkinje and ventricular myocardial cells.

Action potentials of isolated Purkinje cells of dogs and the electrophysiological actions of higenamine on the dog's Purkinje cells were studied by glass microelectrodes. The actions of higenamine on the action potential of Purkinje cells were: (1) increase of amplitude of the plateau phase, (2) enhancement of repolarization of phase 3 and shortening of action potential duration (APD), (3) lower concentration of higenamine (10(-7) g/ml) causing shortening of APD without any significant change of the effective refractory period (ERP), and higher concentration (10(-6) g/ml) of it causing shortening of both APD and ERP, (4) higher concentration (10(-6) g/ml) of higenamine increasing the slope of phase 4, decreasing the threshold of depolarization, and increasing the automaticity of the Purkinje cells, (5) action of higenamine on the Purkinje cells only partially blocked by tetrodotoxin (TTX) and verapamil. The above facts suggest that: (1) higher concentration of higenamine may induce tachyarrhythmias, while lower concentration may prevent arrhythmias; (2) in low concentration of higenamine, there is a relative increase of ERP. Thus, higenamine seems to be safer than isoproterenol in the treatment of bradyarrhythmias.

Action Potentials↗

PubMed1988

Photoinduced removal of nifedipine blockade of Ca2+ entry in different phases of gastric plateau action potential.

Spontaneous electrical and contractile activities of gastric antral smooth muscle preparations were recorded using a modified sucrose gap technique, which allowed for the exposition of the muscle strips to a short-light pulse from a xenon flash lamp. Nifedipine (3 x 10(-8)-10(-7) mol/l) inhibited spontaneous spike potentials, modified the shape of plateau action potentials and suppressed or abolished spontaneous contractile activity of muscle preparations. Short UV-illumination rapidly inactivated nifedipine's action and restored both the shape of action potentials and the amplitude of contractions. The data obtained showed that nifedipine-dependent Ca2+ entry participated in excitation-contraction coupling both during initial depolarization and during the plateau of action potentials. After nifedipine inactivation spike potentials superimposed on plateau action potentials and related high-amplitude phasic contraction were recovered.

Action Potentials↗

PubMed1990

Influence of N-ethylmaleimide on action potential and force of contraction of guinea-pig papillary muscles.

1. Standard microelectrode techniques were used to investigate the influence of N-ethylmaleimide on the action potential, slow response action potential and force of contraction of guinea-pig papillary muscles. 2. N-ethylmaleimide, 3 x 10(-5) to 10(-4) mol l-1, concentration-dependently increased the force of contraction. The positive inotropic effect developed quickly and, with the largest drug concentration, was followed by a progressive decline of the contractile force. The action potential duration was progressively shortened by N-ethylmaleimide. 3. The effects of N-ethylmaleimide were not prevented in the presence of tetrodotoxin 3 x 10(-8) mol l-1 and propranolol 4 x 10(-6) mol l-1 or by a reduction of the Na(+)-concentration to 70 mmol l-1. 4. Verapamil, 10(-6) mol l-1, reduced the positive inotropic, but not the action potential shortening effect of N-ethylmaleimide. 5. In K(+)-depolarized muscles in the presence of propranolol and tetrodotoxin, N-ethylmaleimide 10(-4) mol l-1 increased the maximum depolarization velocity and the duration of the slow response action potential. The latter effect was transient and was followed by a progressive reduction of the action potential duration. 6. The most likely explanation for the action potential shortening effect of N-ethylmaleimide seems to be an increase of an outward potassium current while the transient inotropic effect of the drug may be caused, at least in part, by an increase of the slow inward calcium current.

Action Potentials↗

PubMed1989

Activation of adenylate cyclase by forskolin prolongs calcium action potential duration in lamprey sensory neurons.

Calcium-dependent action potentials of primary sensory neurons in the isolated spinal cord of the lamprey were greatly prolonged in duration by forskolin, an activator of adenylate cyclase in other systems. This effect was dose-dependent over the tested range of 25-400 microM with an EC50 of 55 microM. Experiments were performed to establish a role for adenylate cyclase and adenosine 3',5'-cyclic monophosphate (cAMP) as mediators of the forskolin effect. The prolonging action of forskolin on the Ca action potential was significantly reduced in the presence of the adenylate cyclase inhibitor 2',5'-dideoxyadenosine. The inactive forskolin analogue 1,9-dideoxyforskolin did not prolong the duration of the Ca action potential, while forskolin treatment of the same cells produced a large and rapid increase in action potential duration. In addition, the prolonging action of forskolin was potentiated by the phosphodiesterase inhibitor, theophylline. It is concluded that forskolin acts in lamprey sensory neurons to activate adenylate cyclase and raise intracellular cAMP levels which in turn mediate the increase in Ca action potential duration.

Action Potentials↗

PubMed1976

Tonoplast action potential in Nitella in relation to vacuolar chloride concentration.

The action potential of Nitella internode was studied in relation to K+ and C1- concentrations in the vacuole. When the vacuole of Nitella pulchella was filled with an artificial solution with extremely low C1- concentration, a diphasic action potential (DAP) was observed. T he first phase consists of a rapid depolarization followed by a relatively rapid repolarization, and the second one consists of a strong hyperpolarization followed by a gradual return to the resting potential. When the cell was stimulated immediately after the generation of DAP, a monophasic action potential which resembles an action potential of the natural cell was observed, indicating that the DAP consists of two components with different refractory periods. The refractory period of the component responsible for the depolarizing is shorter than that of a component responsible for the hyperpolarizing phase. Measuring the plasmalemma potential and vascuolar potential separately, it was demonstrated that the hyperpolarizing component of DAP originates from the tonoplast. The action potential of the tonoplast, in contrast with that of the plasmalemma, could be generated independently of concentration of K+ in the vasuole. Since the maximum amplitude of hyperpolarization decreased significantly by increasing C1- concentration of the vacuole, it is concluded that the tonoplast is very sensitive to C1- during excitation.

Action Potentials↗

PubMed1994

Time course of postnatal changes in rat heart action potential and in transient outward current is different.

The rat ventricular action potential shortens after birth. The contribution of increases in the transient outward current (Ito) to postnatal action potential shortening was assessed by measuring Ito in isolated cells and by determining the effect of 2 mM 4-aminopyridine (4-AP) on the action potentials of papillary muscles. 4-AP had no effect on 1-day action potential duration at 25% repolarization (APD25), and 1-day cells had little Ito. In 8- to 10-day muscles, 4-AP caused a small, but significant, increase in APD25. Ito increased slightly between day 1 and days 8-10, but this increase was not significant. Most of the increase in Ito (79%) and in the response to 4-AP (64%) occurred between days 8-10 and adult; however, approximately 75% of the APD25 shortening took place by days 8-10. Thus, while Ito may contribute to repolarization in late neonatal and adult cells, the different time courses of action potential shortening and increases in Ito suggest that changes in Ito are unlikely to be responsible for most of the postnatal action potential shortening.

4-Aminopyridine↗

PubMed1989

Frequency- and voltage-dependent effects of recainam on the upstroke velocity of action potential in rabbit ventricular muscle.

The effects of recainam (Wy 42,362) on transmembrane action potentials were examined in isolated rabbit right ventricular papillary muscles. Recainam (3 x 10(-5) to 3 x 10(-4) M) caused a concentration-dependent decrease in the Vmax of the action potential. At 3 x 10(-4) M, there was a slight decrease in the amplitude of the action potential. The resting potential and the action potential duration were not affected. Use-dependent block of Vmax was tested over a wide range of pacing frequencies (from 0.1 to 3.0 Hz). At 1.0 Hz, recainam 10(-4) M produced exponential decreases in Vmax with a rate constant of 0.17 per action potential and 39.8% reduction at steady state. This use-dependent block was augmented at the higher stimulation frequencies. The time constant for the recovery of Vmax from use-dependent block (offset) was 17.2 s. In papillary muscles depolarized with 10 mM [K+]0, the use-dependent block was augmented but tonic block and the rates of onset and offset of the use-dependent block were similar to those in normally polarized preparations in 4 mM [K+]0. The curves relating membrane potential and Vmax in preparations stimulated at a low frequency (0.01 Hz) were not shifted by 10(-4) M recainam. These findings suggest that recainam is a specific sodium-channel blocker and has kinetically slow but potent affinity for the channel during action potentials. This selective binding during action potential was further augmented by depolarization and is likely to play a significant role in the control of ventricular arrhythmias by the drug.

Action Potentials↗

PubMed1988

Effects of exogenous ubidecarenone on cardiac action potential and activation time in hypoxic, glucose-free solution. Possible antiarrhythmic action of ubidecarenone.

Effects of ubidecarenone (coenzyme Q10, CoQ10, E-0216) on the cardiac action potential depressed by the superfusion with hypoxic, glucose-free solution (modified Tyrode solution) and on the activation time (ACT) altered by the same means were investigated. In the control specimens, the action potential duration (APD) was markedly shortened and action potential amplitude (AMP) reduced. The maximum rate of rise of phase zero Vmax) and the resting membrane potential (RMP) were slightly affected. Superfusion with exogenous CoQ10 significantly reversed the depressed APD and AMP, and tended to increase RMP and Vmax. Moreover, the ACT which, in the control, was slightly shortened until after the 10th min of superfusion became progressively longer. It was slightly prolonged during the first 10 min, and from the 12th to the 15th min was slightly shortened by treatment with CoQ10. These results suggest that CoQ10 could evoke an antiarrhythmic action in cardiac cells in depressed metabolic conditions.

Action Potentials↗

PubMed1996

Effects of halothane and isoflurane on rat ventricular action potentials recorded in situ.

The effects of halothane and isoflurane on ventricular intracellular action potentials recorded in situ in pentobarbital anesthetized rats were studied. Halothane (0.5, 1 and 2 vol.%) and isoflurane (0.75, 1.5 and 3 vol.%) did not have identical effects on rat epicardial action potentials recorded by floating microelectrodes. However, over the concentration range tested, both anesthetics reduced blood pressure and heart rate to a similar extent. Isoflurane did not effect the maximum rate of rise of the action potential amplitude. However, 3 vol.% isoflurane reduced the resting membrane potential from -72+/-2 to -65+/-3 mV (mean+/-SEM, p<0.05) while the highest concentration of halothane had no effect. Halothane (2 vol.%) reduced action potential amplitude from 74+/-4 to 65+/-3 mV (p<0.05) and reduced the maximum rise rate of action potential from 175+/-21 to 133+/-8 V/s (p<0.05). Both isoflurane and halothane prolonged action potential duration at 10, 25 and 50% repolarization while only halothane significantly shortened action potential duration at 75% repolarization, Thus the effects of halothane and isoflurane on ventricular transmembrane action potentials were similar, but not identical. The relevance of such observations to the antiarrhythmic actions of halothane, but not isoflurane in this species is not clear.

Action Potentials↗