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PubMed1995

Effects of action potential duration on excitation-contraction coupling in rat ventricular myocytes. Action potential voltage-clamp measurements.

Although each of the fundamental processes involved in excitation-contraction coupling in mammalian heart has been identified, many quantitative details remain unclear. The initial goal of our experiments was to measure both the transmembrane Ca2+ current, which triggers contraction, and the Ca2+ extrusion due to Na(+)-Ca2+ exchange in a single ventricular myocyte. An action potential waveform was used as the command for the voltage-clamp circuit, and the membrane potential, membrane current, [Ca2+]i, and contraction (unloaded cell shortening) were monitored simultaneously. Ca(2+)-dependent membrane current during an action potential consists of two components: (1) Ca2+ influx through L-type Ca2+ channels (ICa-L) during the plateau of the action potential and (2) a slow inward tail current that develops during repolarization negative to approximately -25 mV and continues during diastole. This slow inward tail current can be abolished completely by replacement of extracellular Na+ with Li+, suggesting that it is due to electrogenic Na(+)-Ca2+ exchange. In agreement with this, the net charge movement corresponding to the inward component of the Ca(2+)-dependent current (ICa-L) was approximately twice that during the slow inward tail current, a finding that is predicted by a scheme in which the Ca2+ that enters during ICa is extruded during diastole by a 3 Na(+)-1 Ca2+ electrogenic exchanger. Action potential duration is known to be a significant inotropic variable, but the quantitative relation between changes in Ca2+ current, action potential duration, and developed tension has not been described in a single myocyte. We used the action potential voltage-clamp technique on ventricular myocytes loaded with indo 1 or rhod 2, both Ca2+ indicators, to study the relation between action potential duration, ICa-L, and cell shortening (inotropic effect). A rapid change from a "short" to a "long" action potential command waveform resulted in an immediate decrease in peak ICa-L and a marked slowing of its decline (inactivation). Prolongation of the action potential also resulted in slowly developing increases in the magnitude of Ca2+ transients (145 +/- 2%) and unloaded cell shortening (4.0 +/- 0.4 to 7.6 +/- 0.4 microns). The time-dependent nature of these effects suggests that a change in Ca2+ content (loading) of the sarcoplasmic reticulum is responsible. Measurement of [Ca2+]i by use of rhod 2 showed that changes in the rate of rise of the [Ca2+]i transient (which in rat ventricle is due to the rate of Ca2+ release from the sarcoplasmic reticulum) were closely correlated with changes in the magnitude and the time course of ICa-L.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed2006

Monophasic action potentials and activation recovery intervals as measures of ventricular action potential duration: experimental evidence to resolve some controversies.

BACKGROUND: Activation recovery intervals (ARIs) and monophasic action potential (MAP) duration are used as measures of action potential duration in beating hearts. However, controversies exist concerning the correct way to record MAPs or calculate ARIs. We have addressed these issues experimentally. OBJECTIVES: To experimentally address the controversies concerning the correct way to record MAPs or calculate ARIs. METHODS: Left ventricular local electrograms were recorded in isolated pig hearts with an exploring electrode grid, with a KCl reference electrode on the left ventricular myocardium, the aortic root, or the left atrium. Local activation was determined from calculated Laplacian electrograms. RESULTS: With the KCl electrode on the aortic root, local electrograms represented local activation. However, with the KCl electrode on the myocardium remote from the exploring electrode, a combined electrogram emerged consisting of local activation recorded from the grid and remote activation recorded from the reference electrode. The remote, inverted monophasic component did not show propagation and did not correlate with the Laplacian complex. When the KCl electrode was placed on the atrium during AV block, remote atrial monophasic components were completely dissociated from local, ventricular deflections. At left ventricular sites with a positive T wave, the Laplacian signal showed that the end of the T wave was caused by remote repolarization. During cooling-induced regional action potential prolongation, the T wave became negative, whereby the positive flank of the T wave remained correlated with repolarization (recorded with a MAP at the same site). CONCLUSIONS: MAPs are recorded from the depolarizing electrode. In both negative and positive T waves, the moment of maximum dV/dt corresponds to local repolarization.

Action Potentials↗
PubMed1987

A study of electrical activation of the heart by laser spectrometry. An optical study of cellular action potentials.

The action potentials of working myocardium and conduction tissues, traditionally recorded by intracellular glass microelectrodes, may also be studied at a distance without physical contact using an optical system. The tissues have to be stained with a dye which fluoresces when illuminated by a laser beam, and the spectrum of the fluorescence must be sensitive to variations of the transmembrane action potential. The responses obtained by the microelectrode and the optical systems were tested on several different preparations (sheep and mouse myocardium). Three types of signals were obtained: asynchronous, synchronous and mixed, related to myocardial contraction, the action potential and the excitation-contraction couple, respectively. The use of continuous and pulsed mode laser measurements by optoelectronic methods (photomultiplier, monochromator), and imaging of the electrical activation by a CCD video camera may lead to the development of high definition mapping of myocardial activation which would be used for studying arrhythmias in experimental and even clinical models.

Action Potentials↗
PubMed1983

Potentiation of slow action potentials with theophylline or "micro" adenosine deaminase.

The effects of endogenous adenosine on rat atrial and ventricular slow action potentials (AP) were studied using theophylline, an adenosine receptor antagonist, or "micro" adenosine deaminase (mADA), small polypeptides having adenosine deaminase activity. Exogenous adenosine (10(-6) M) depressed slow APs at low and high isoproterenol concentrations and shifted the isoproterenol dose-response curve to the right in the atrium. In the ventricle, exogenous adenosine inhibited slow APs at low isoproterenol doses and only shifted the bottom of the dose-response relationship to the right. mADA (0.84 U) or theophylline (5 X 10(-5) M) potentiated the response to threshold concentrations of isoproterenol and caused a parallel shift of the curve to the left in the atrium but only shifted the bottom portion of the curve in the ventricle. This potentiation of slow APs in the presence of mADA or theophylline suggests that endogenous adenosine attenuates the response to isoproterenol in cardiac muscle.

Action Potentials↗
PubMed1982

Barbiturate reduction of calcium-dependent action potentials: correlation with anesthetic action.

Calcium-dependent action potentials were recorded from mouse spinal cord neurons in primary dissociated cell culture following addition of the potassium channel blockers tetraethylammonium ion and 3-aminopyridine. The pharmacologically active barbiturates, pentobarbital and phenobarbital, but not the pharmacologically inactive barbiturate, barbituric acid, produced reversible, dose-dependent reduction of action potential duration at sedative-hypnotic and anesthetic concentrations. Pentobarbital reduced action potential duration at concentrations from 25 to 600 microM (50% reduction at 170 microM) while phenobarbital reduced action potential duration at concentrations from 100 to 5000 microM (50% reduction at 900 microM). The barbiturate concentrations which reduced calcium-dependent action potential duration in this study correlate with reduction of neurotransmitter release from other neuronal preparations and with reduction of calcium uptake by synaptosomes. The results suggest that barbiturates may produce anesthesia in part by reduction of presynaptic calcium entry and consequent reduction of neurotransmitter release in addition to postsynaptic increase of membrane chloride ion conductance. Barbiturate anticonvulsant actions are probably due to postsynaptic augmentation of GABA-mediated inhibition and depression of excitatory synaptic transmission. The major difference between anticonvulsant (phenobarbital) and anesthetic (pentobarbital) barbiturates was the dose-dependency of these actions. Phenobarbital produced postsynaptic modulation of neurotransmitter responses at low concentrations and decreased calcium-dependent action potential duration and increased chloride ion conductance at high concentrations. In contrast, pentobarbital produced all actions at low concentrations. Thus for phenobarbital there would be a large therapeutic index for anticonvulsant activity compared to anesthetic activity but for pentobarbital there would be a small therapeutic index.

Animals↗
PubMed1979

Anemone toxin discriminates between ionic channels for receptor potential and for action potential production in a sensory neuron.

The effect of anemone toxin (ATX II), which slows sodium channel inactivation at electrically excitable membranes, was investigated in the slowly adapting stretch receptor organ of crayfish. The toxin affected the action potentials, but produced no changes in the stretch induced receptor potentials. This finding is further proof for the high selectivity of this toxin molecule for sodium channels which are gated by membrane depolarissations.

Action Potentials↗
PubMed1994

Nerve compound action potentials analysed with the simultaneously measured single fibre action potentials in humans.

1. Compound action potentials (APs) and single fibre APs were recorded with two pairs of wire electrodes from an S5 root from a paraplegic patient during surgery. 2. Frequency distribution histograms of single nerve fibre conduction velocities were constructed and nerve fibre group conduction velocities compared with the conduction velocities of the peaks of the compound APs. By increasing the strength of the stimulation, the peaks in the compound AP could be identified, and the threshold order of efferent nerve fibre groups determined. Using additional literature data, it is likely that the primary spindle afferents have the lowest threshold due to electrical nerve root stimulation followed by the alpha 1-motoneurons (FF), the secondary muscle spindle afferents, the alpha 2-motoneurons (FR), the alpha 3-motoneurons (S), the gamma beta, gamma 1 (dynamic), gamma 21 (static), gamma 22 (static), and the parasympathetic motoneurons. 3. In first approximations, the Ap duration increases in the same way as the AP amplitude decreases with decreasing conduction velocity, and the area between the average single fibre AP curve and the base-line is the same for all single fibre APs with an average same distance to the recording electrodes in the root cross-section. By comparing the mean area of a single fibre AP with the areas of the peaks of the compound APs, it was found that 230 single fibre APs contributed to the compound AP. In the secondary spindle afferent fibre and alpha 2-motoneurons groups 53 fibres were stimulated (23%). The alpha 3-motoneuron peak and the afferents in the same velocity range contained 101 fibres (44%), the gamma beta peak contained 9 fibres (4%), the gamma 1 32 (14%), the gamma 21 23 (10%) and the gamma 22 12 (5%) fibres. Additionally two primary spindle afferents and two alpha 1-motoneurons most likely contributed to the compound AP. Since the large peaks in the compound APs did not change their area with increasing stimulation, most likely all muscle spindle afferents and alpha-motoneurons were activated to contribute to the compound AP. 4. Transfer functions of nerves and the stimulation with natural impulse patterns of the adequate afferents to spinal oscillators with respect to continence in paraplegia are discussed.

Action Potentials↗
PubMed1984

Effects of the calmodulin inhibitor, trifluoperazine, on membrane potentials and slow action potentials of cultured heart cells.

The effects of an inhibitor of calmodulin, trifluoperazine (TFP), were determined on the electrical activity of cultured cell reaggregates derived from chick embryonic hearts (15-day-old). The cells exhibited naturally occurring slowly rising action potentials (APs) having a maximum rate of rise (+Vmax) of less than 35 V/s. After superfusion with 100 microM TFP, the maximal diastolic potential (MDP) decreased, within 30 min, from -66.0 to -55.5 mV. The frequency of discharge decreased, and there was also a decrease in AP amplitude and in +Vmax (from 10.0 to 4.9 V/s). By 90 min, all spontaneous activity had stopped, and the resting potential was about -10 mV. Input resistance increased, consistent with a decrease in K+ conductance. Hyperpolarization by current pulses did not allow the production of APs upon electrical stimulation, suggesting that the TFP blocks slow inward current (Isi). No recovery occurred upon washout (up to 48 h). Higher concentrations of TFP (200-500 microM), or injection of the inhibitor intracellularly be means of phosphatidylcholine liposomes, accelerated the time course of the blockade (e.g. within 15 min). In fresh (non-cultured) chick ventricle with fast-rising APs, TFP (400 microM) caused excitation-contraction uncoupling within 10 min, presumably by blocking the slow Ca2+ channels; the the fast APs were depressed (+Vmax) within 45 min, before any depolarization occurred. The cells became completely depolarized (Em congruent to -4 mV) by 195 min; hyperpolarization by current pulses did not allow the production of APs, suggesting that the fast Na+ channels were blocked.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1994

A dynamic model of the cardiac ventricular action potential. II. Afterdepolarizations, triggered activity, and potentiation.

The action potential model presented in our accompanying article in this journal is used to investigate phenomena that involve dynamic changes of [Ca2+]i, as described below. Delayed afterdepolarizations (DADs) are induced by spontaneous Ca2+ release from the sarcoplasmic reticulum (SR), which, in turn, activates both the Na(+)-Ca2+ exchanger (INaCa) and a nonspecific Ca(2+)-activated current (Ins(Ca)). The relative contributions of INaCa and of Ins(Ca) to the generation of DADs are different under different degrees of Ca2+ overload. Early afterdepolarizations (EADs) can be categorized into two types: (1) plateau EADs, resulting from a secondary activation of the L-type Ca2+ current during the plateau of an action potential, and (2) phase-3 EADs, resulting from activation of INaCa and Ins(Ca) by increased [Ca2+]i due to spontaneous Ca2+ release from the SR during the late repolarization phase. Spontaneous rhythmic activity and triggered activity are caused by spontaneous Ca2+ release from the SR under conditions of Ca2+ overload. Postextrasystolic potentiation reflects the time delay associated with translocation of Ca2+ from network SR to junctional SR. The cell is paced at high frequencies to investigate the long-term effects on the intracellular ionic concentrations.

Action Potentials↗
PubMed1985

Modulation at the guinea pig round window of summating potentials and compound action potentials by low-frequency sound.

Low-frequency sound was used to modulate responses to short single-frequency tone bursts at the guinea pig round window. Summating potentials (SP) increase (reach higher positive values) during the negative half-cycle of the low-frequency cochlear microphonic (LFCM) and decrease during the positive half-cycle of the LFCM. The compound action potential (AP) amplitude decreases during the negative half-cycle of the LFCM. The negative half-cycle of the LFCM can be identified with scala tympani displacement. SP modulation depth is defined as the difference between the highest and the lowest SP value found for tone burst stimulation at different phases of the low-frequency sound while the sound levels of the tone burst and the low-frequency bias are kept constant. When normalized with respect to the SP amplitude found without bias, the SP modulation depth is independent of the sound level of the tone burst in the range from 48 to 68 dB SPL. The normalized AP suppression tends to increase with decreasing tone burst sound level. A dynamic nonlinear mechanism which might explain these results is discussed. This mechanism is based on voltage-sensitive changes.

Acoustic Stimulation↗
PubMedDate not supplied

Effects of a newly synthetized calcium antagonist, cyclopropylmethyl 4-(3-nitrophenyl) 1,4-dihydro-2,6-dimethylpyridine-3,5-dicarboxylate (MPC-2101), on action potentials of rabbit's myocardial tissues in vitro.

Electrophysiological effects of cyclopropylmethyl 4-(3-nitrophenyl) 1,4-dihydro-2,6-dimethylpyridine-3,5-dicarboxylate (MPC-2101), a newly synthetized compound, were examined in the rabbit SA node and papillary muscle, using a conventional microelectrode technique in vitro. In the SA node, MPC-2101 (10(-8) - 10(-6) M) showed dose-dependent negative chronotropic effects by depressing the slope of slow diastolic repolarization without significant effects on maximum diastolic potential and action potential duration. MPC-2101 (10(-7) - 10(-5) M) had no significant effects on the resting membrane potential, the amplitude and dV/dt of action potentials in papillary muscles, but induced a statistically significant reduction of the plateau phase of the action potential duration measured at 20% repolarization at a concentration of 10(-5) M. MPC-2101, at concentrations lower than 10(-6) M, had no significant effects on the amplitude, dV/dt, or duration of slow action potentials induced in 18 mM (K+]o and histamine at 10(-6) M, but at 3 x 10(-6) M significantly depressed all parameters of the slow action potentials. In higher Ca2+ solution, dose-response curves for MPC-2101 on dV/dt of slow action potentials were shifted to the right. MPC-2101, at a concentration of 3 x 10(-6) M, showed frequency-dependent depression in dV/dt of the slow action potentials. MPC-2101 showed less potent actions than nicardipine on electrophysiological activities of the SA node and papillary muscle.

Action Potentials↗
PubMed1989

Effects of AFD-21, a new class I antiarrhythmic agent, and AFD-19, its active metabolite, on the maximal rate of rise of action potentials in guinea pig papillary muscles: dependence on time, voltage, and action potential duration.

Effects of AFD-21 and AFD-19 (a new class I antiarrhythmic agent and its active metabolite, respectively) on the maximal rate of rise (Vmax) of action potentials (APs) were studied in guinea pig papillary muscles with special reference to their time, voltage, and action potential duration (APD) dependence. Both AFD-21 and AFD-19 (2-10 microM) reduced Vmax in a concentration-dependent manner without affecting the resting potential, APD, and effective refractory period. Both agents (5 microM) shifted the normalized Vmax resting potential curve (examined at 1 Hz) in the hyperpolarizing direction by 4-7 mV (voltage dependence). In addition, both agents (5 microM): a) caused a frequency-dependent reduction of Vmax at 0.25-3 Hz; b) developed a use-dependent (1 Hz) reduction of Vmax with an onset time constant of 1-3 s; and c) slowed the recovery process of Vmax, whose resultant recovery time constant was 2-3 s (time dependence). Nicorandil (1 mM), which shortens APD to about 25% of control, antagonized the AFD-21-induced time-dependent reductions of Vmax but not the AFD-19-induced reductions (APD dependence). These results suggest that the effects of AFD-21 on Vmax are APD dependent but those of AFD-19 are not, and thereby that AFD-21 and AFD-19 preferentially block inactivated and open sodium channels, respectively. The present findings are discussed from the viewpoint of the modulated or the guarded receptor hypothesis.

Action Potentials↗
PubMed1983

Optical evidence for calcium-action potentials in early embryonic precontractile chick heart using a potential-sensitive dye.

Using an optical method for monitoring membrane potential, spontaneous action potentials in the 7- to 9-somite embryonic precontractile chick hearts were measured. The optical action potential in the 7- to 9-somite embryonic heart was lacking 'phase 0' and 'phase 1' attributable to the fast Na+ current. The embryonic precontractile heart continued to generate spontaneous action potentials in a Na+-free solution or in the presence of tetrodotoxin. Such an action potential was blocked by adding Co2+, Mn2+, Ni2+, La3+, D-600 or GEDTA, and the frequency, the amplitude, and the rate of rise of the spontaneous action potentials depended closely upon the external Ca2+ concentration; reducing the external Ca2+ concentration resulted in suppression of the spontaneous excitability. From the above results, we concluded that the spontaneous action potential in the early phases of cardiogenesis is characterized as a Ca2+-dependent action potential.

Action Potentials↗
PubMed1999

Non-invasive detection of the single motor unit action potential by averaging the spatial potential distribution triggered on a spatially filtered motor unit action potential.

For research as well as diagnostic applications the non-invasive detection of the activity of single motor units is of interest. The most direct information is expected to be found in monopolarly recorded data. But when an array of surface electrodes is used for the monopolar recordings of the potential distribution on the skin, in most cases an additional invasive needle electrode is utilized to detect the exact points in time when a certain motor unit is firing. With this supplementary information, an averaging of the monopolar EMG tracings can be performed. In this paper, a completely non-invasive methodology is presented which replaces the invasive needle by a spatial filtering procedure. The EMG signals from the m. biceps brachii are recorded monopolarly with an electrode array. Afterwards, a spatial filtering procedure, called normal double differentiating filter, is applied to the data. The EMG signals obtained are investigated by means of an amplitude threshold to distinguish the activity of different motor units. The point of the maximum amplitude of the selected peaks then is used as trigger point to average the monopolar EMG data. The time courses of the motor unit action potential signals found after applying the described procedure show similar shapes, while two different components are to be identified: corresponding to the spread of the excitation, one is referring to stationary, the other to travelling events. These results justify the possibility to replace the needle electrode to obtain a trigger event in the future by the non-invasive spatial filtering procedure.

Action Potentials↗
PubMed1995

Multiple effects of salicylaldoxime on rat cardiac action potentials.

The effect of salicylaldoxime, 2-(OH)C6H4CH = NOH, on the resting membrane potential and action potential characteristics was studied using isolated right ventricular strips from rat heart. Salicylaldoxime (1-3 mM) reversibly hyperpolarized the cells, increased action potential amplitude, decreased the maximal rate of rise (Vmax) and prolonged duration. The prolongation of the action potential produced by 1 mM salicyaldoxime could not be reversed with isoprenaline (10 microM). Salicyalaldoxime (0.3-1 mM) had no effect on the Ca(2+)-dependent slow action potential for periods up to 60 min. Initial exposure to 3 mM salicylaldoxime produced no changes in the slow action potential, but after 30 min. there was a gradual reduction in amplitude. This effect was completely reversible within 10-15 min. of washout. These data suggest that salicyaladoxime can block Na+, K+ and Ca2+ currents in rat cardiac muscle. Furthermore, it appears that the slow inward Ca2+ current, as measured by the slow action potential, may be sensitive to a dephoshorylating action of this oxime.

Action Potentials↗
PubMed1982

Ionic events responsible for the cardiac resting and action potential.

The cardiac action potential is distinguished from other excitatory phenomena by a prominent plateau and by the latent pacemaking capability of cardiac muscle. A review of experimental data suggests that ionic fluxes through gated membrane channels are the primary determinants of the shape of the cardiac action potential. The rapid depolarization phase of the action potential is mediated in part by an ionic channel that resembles the sodium ion (Na+) channel of nerve. A slower channel capable of carrying both calcium ion (Ca2+) and Na+ currents (Isi) also contributes to the upstroke of the action potential. The Ca2+ current through this channel is partly responsible for maintaining the plateau phase of the action potential. Moreover, because this slower channel activates at more positive potentials in partly depolarized myocardium or in specialized conduction tissue such as the sinoatrial and atrioventricular nodes. Two distinct transport systems appear to be the principal regulators of potassium ion (K+) in myocardium. An inwardly rectifying, voltage-dependent K+ channel apparently maintains all K+ conductance at rest and at all potentials negative to --20 mV. A second channel, which is both voltage- and time-dependent, evidently mediates K+ flux during the plateau phase of the action potential. This K+ current activates at potentials positive to --20 mV. The role of coupled transport mechanisms is now well established. The low intracellular concentrations of Na+ and Ca2+ prevailing in the myocardium are maintained by an electrogenic Na+ pump and a Na+-Ca2+ counter-transport system. Current data on carrier-mediated transport systems are insufficient to delineate the role of such mechanisms in the control of cardiac action potential. Further studies are required to provide details of the voltage, temporal and ionic dependence of gated channels, as well as of ionic counter-transport carriers, so that a quantitative reconstruction of cardiac action potential may be attempted.

Animals↗