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Biomedical subjects

B Nilius

Publications and source records attributed to B Nilius.

At least 235 records · Page 13Linked to original sources
PubMed1983

Dependence of muscarinic effects of acetylcholine in mammalian atrial myocardium on the external calcium and potassium concentration.

Action potentials were recorded from isolated atrial trabeculae of the rabbit using a standard microelectrode technique and analyzed by a phase-plane technique. Muscarinic effects of acetylcholine (ACh) were studied in verapamil-containing solutions (13.2 mumol/l). The shortening of the action potentials by ACh was accentuated in high K+ solutions but depressed in Ca++ excess solutions. ACh-induced conductance was found to be concentration-dependent. From the concentration conductance plots a Hill coefficient of 1 was obtained under all the conditions tested. The maximum conductance calculated from the concentration-conductance plots varied between 11.3 +/- 2.7 microS/cm2 (at 7.5 mmol/l Ca++, 2.7 mmol/l K+ in the external solution) and 46.4 +/- 5.0 microS/cm2 (at 0.1 mmol/l Ca++, 8.1 mmol/l K+). All the effects on the ACh-induced conductance could be described by the reaction scheme for the nicotinic ACh action. From both the experimental findings and the approximation of the measurements using the Katz-Miledi model it is suggested that an increase in the external K+ concentration increased, but an external Ca++ excess decreased, the conductance of the ACh-induced channel.

Acetylcholine↗
PubMed1983

Desensitization of the muscarinic receptor in the mammalian atrial myocardium.

Action potentials of constantly driven isolated trabeculae of the rabbit's atrial myocardium, being depressed by acetylcholine (ACh) at concentrations between 0.2 and 20 mumol/l, recovered during a constant drug application. The sensitivity of the atrial myocardium to ACh after a prolonged drug application was decreased but found to be restored about 7 min after switching off the ACh superfusion. The recovery during drug application was accelerated in Ca++ excess solutions but decelerated in K+ excess solutions. All the effects of ACh were blocked by atropine (1 mumol/l) completely. The results suggest that the muscarinic ACh receptor in the mammalian myocardium, responsible for the electrotropic effects, shows desensitization to ACh similar to the nicotinic receptor in other tissues.

Acetylcholine↗
PubMed1983

Rabbit atrial myocardium in hypoxic conditions: rate dependent variation of action potential.

The dependence of the repolarization phase of the action potential in the atrial myocardium on the pacing pattern was studied in normoxic and hypoxic conditions. Intracellular action potentials were recorded by means of the conventional microelectrode technique from isolated left atrial trabeculae of the rabbit. By varying the pacing pattern and the oxygen supply changes of the configuration of action potential and of the membrane current as well as a conductance measure gK were obtained. In all pacing patterns the duration of action potentials is shortened, and the net outward current is enhanced by hypoxia. In steady state and for premature action potentials, gK is enlarged by hypoxia, but in action potentials after a pacing pause it is diminished more in hypoxic than in normoxic conditions. The findings suggest inhibition of an inward current in hypoxia as well as a dependence of a potassium background conductance on the inner Ca-concentration in normoxic and hypoxic conditions.

Action Potentials↗
PubMed1983

Pacing dependent properties of the transmembrane potential in plateau-fibres of the mammalian atrial myocardium.

The effects of cycle length (CL) alteration on action potentials of isolated trabeculae of the common right atrial working myocardium (M) and isolated preparation of the crista terminalis (CT) of the rabbit heart were studied. Prolonging the CL increased the steady state duration of action potentials in M but decreased it in CT fibres. The repolarization of the post-pause action potentials of the M preparations was characterized by (i) a rapid initial repolarization followed by (ii) a plateau phase and (iii) a retarded terminal repolarization. In CT fibres the retarded repolarization was not observed and the duration of the post-pause action potentials at 90% repolarization is decreased. Premature action potentials of the M preparations were shortened at 90%, but were prolonged at 25% repolarization. Premature action potentials of the CT fibres were prolonged. The post-drive resting transmembrane potential of the M preparations moved to more negative values depending on the CL stimulation. The shift of the post-drive transmembrane resting potential to negative values in CT preparations was preceded by an initial depolarization. The initial depolarization was absent in M preparations. Myofibril-poor pale cells were found consistently in CT, but never in M preparations.

Action Potentials↗
PubMed1982

Does a calcium-mediated outward current exist in the atrial myocardium?

Using a microelectrode technique the influence of experimental conditions which are known to alter the intracellular free Ca concentration upon the repolarization phase in the rabbit atrial myocardium was studied. Under all the tested conditions (increased external Ca concentration, application of ouabain, decreased external K concentration) a positive inotropic effect was observed. The action potentials showed a rapid initial repolarization. The positive inotropic effect was found to be well correlated with the effect of the action potential's shortening at 25% repolarization. After pacing pauses a positive correlation between the velocity of the initial rapid repolarization and the potentiation of the atrial contraction was established. It is discussed that all the conditions were able to increase the internal Ca concentration and that in consequence of it a CA-sensitive outward current at potentials about 40 mV more positive than the resting potential is activated.

Action Potentials↗
PubMed1981

Properties of an acetylcholine-induced conductance in the rabbit atrial myocardium.

Using a conventional microelectrode technique, action potentials (A.P.) recorded from the isolated left atrial trabeculae of the rabbit were analyzed. The membrane current during A.P. was reconstructed. In spite of an extracellular Ca2+-deficiency and the application of verapamil, acetylcholine (ACh) reduced the A.P. duration by inducing an outward current IACh. This current was blocked by atropine (10-6 M). A Nernst-plot of the reversal potential at different K+-concentrations showed a slope of 58.5 mV for a 10-fold change in concentration. After pacing pauses longer than 10 s an inward going (anomalous) rectification (A.R.) for IACh occurred. Increasing the duration of the pacing pauses the rectification was more accentuated. During a constant pacing the A.R. for IACh disappeared. ACh did not modify the A.R. The maximum slope conductance for IACh was dependent on the extracellular concentration of ACh (0.035 mS x cm-2 at 20 microM ACh, 0.012 mS x cm-2 at 0.2 microM ACh). The experimental results are discussed, using the model of an ACh-induced potassium channel. The channel should be related to the muscarinic receptor of the atrial myocardium.

Acetylcholine↗
PubMed1981

[Properties of the premature extrasystolic action potentials in the rabbit atrial myocardium].

Using a conventional microelectrode technique premature action potentials of left auricular trabeculae of the rabbit were studied. Varying the delay between a regular stimulus and the following premature stimulus the duration of the premature action potential (A. P.) is decreased during the relative refractory period and increased after this time at each level of the repolarization. Verapamil suppresses completely this augmentation of the A. P. duration. Turning to account the A. P. measurements an estimation of a potassium conductivity gK yields an enlargement of gK during the premature A. P. elevating the Ca+ concentration or prolonging the steady state pacing interval the increase of gK is more accentuated. Low Ca++ solutions and verapamil suppress the augmentation of gK during the premature A.P. lead to a membrane current responsible for the premature changes of the A. P. This current is inward directed at potentials more positive than --30 mV and outward directed at more negative potentials. By application of high-calcium solutions and in slow pacing both the inward and outward component are increased. The findings suggest an augmented Ca++ inward current during the premature action related to the postextrasystolic potentiation.

Action Potentials↗
PubMed1981

Parasympathetic influence on electrical vulnerability in the atrial myocardium of the rabbit.

Repetitive activity of the isolated rabbit atrium was induced by trains of premature stimuli. Analyzing the interval-histograms of the recorded atrial action potentials a quantitative description of this arrhythmia is demonstrated. An atrial flutter or fibrillation is evoked 110 to 140 ms after a regular driving pulse. Vagal stimulation increases the electrical vulnerability. The degree of arrhythmia was found to be dependent on the frequency of stimulation. During increased vagal activity premature stimuli applied 40 to 190 ms after a regular driving pulse generate arrhythmias. By vagal stimulation a preexisting arrhythmia is converted into an atrial fibrillation. In spite of a constant pacing, the atrial arrhythmia disappears at atrial masses of below 55 mg if initiated by early coupled beats. During an application of acetylcholine this critical mass is reduced.

Action Potentials↗
PubMed1980

[Numerical analysis of myocardial action potentials].

A numerical method is described suitable to reconstruct the repolarization phase of the action potential measured from the mammalian atrial myocardium. The method allows an estimation of the current-voltage relationship of a time-independent potassium outward current and a voltage- and time-dependent calcium current, an inactivation term of the calcium current and an estimation of the calcium and potassium amounts transported during the action potential. The numerical evaluation needs some pairs of voltage-time values obtained from the measured action potentials and the first time derivative of the action potential. An example of the method's usefulness is demonstrated. The described method is suitable to reconstruct the late repolarization phase of the atrial action potentials sufficiently.

Acetylcholine↗
PubMed1980

Stretching-induced changes in the action potential of the atrial myocardium.

The paper reports on changes of the configuration of the action potential recorded from atrial trabecular preparations of the rabbit. Trabeculae, which were isolated from the right atrial cavum (initial length between 2.6 and 5.4 mm) were stretched up to 160% of the initial length. After stretching the steady state action potentials were analysed. While increasing the trabecular length, the duration of 90% repolarization was prolonged and the duration of 25% repolarization was shortened drastically. The conductance for a time-independent potassium outward current gK, measured from the trajectories of the repolarization phase of the action potential, was reduced by increasing the trabecular length. The reconstruction of the measured action potential suggests an increased anomalous rectification for the time-independent potassium current, a decreased amount of the inward transported calcium during the action potential, and a more rapid inactivation of the Ca++-inward current by stretching the atrial myocardium. The results concerning the gK and the anomalous rectification for the potassium current may explain the alleviated generation of the extrasystoles and arrhythmias in the stretched atrial myocardium. The reduction of the Ca++-transport during the action potential may be a control mechanism protecting the heart tissue from the destabilizing effect of an increased anomalous rectification for a time-independent potassium current.

Action Potentials↗
PubMed1980

[Modification of inotropic vagus action by stretching of the heart atrium].

Isolated vagal innervated left rabbit atria were used to study the dependence of inotropic vagal action on the stretching of the auricle myocardium. Pressure-volume relationships, relationships between isovolumetric maxima, inotropic vagal action and filling of the auricle were made on the isolated, vagal-innervated auricles electrically driven by a constant frequency. Pressure-volume relationships and relationships of the isovolumetric maxima are described by means of a model, likewise the dependence of extra-pressure and extra-tension on the volume of the auricle, that is, on the filling pressure. The extra-pressure, derived from the auricle, is at its maximum when a volume of 152% of the volume at a filling pressure of 1 mm Hg is reached. When increasing the filling pressure, both the inotropic action of the vagal stimulation and the inotropic effect of an acetylcholine application decrease. Maximum vagal and acetylcholine action was obtained at filling pressures of 12-16 mm Hg. At a filling pressure of 38 mm Hg only 40% of the maximum vagal action was obtained.

Acetylcholine↗
PubMed1980

[Potentiation and staircase phenomena in rabbit heart atrium and their connection with inotropic vague effects].

At spontaneously beating rabbit atria in vitro longtime pauses of contraction were produced by vagal stimulation. After finishing the stimulation at once contractions took place; the first of them was potentiated. During the vagal pauses various beat interval programs were realized. After removing the sinusoidal node the same programs were repeated by variation of drive interval length. Their effects were compared to the effects in vagal pauses. All these effects were simulated by a two stores three phases model. This model allows description of potentiation and staircase phenomena as well as inotropic vagal effect and inotropic vagal escape. It suggests a connection between this two kinds of phenomena.

Animals↗
PubMed1980

[Pacing-interval-dependent changes of action potentials in the heart atrium of the warm-blooded animal].

Investigated are the cellular post rest action potentials of the rabbit atrial trabeculae (length 2-4 mm, diameter 150-800 micrometers). The first action potential (A.P.) after a pacing pause develops a characteristic configuration: (1) a rapid early repolarization up to -30 to -60 mV within 4 to 8 ms, (2) an extremely decelerated repolarization phase or a secondary depolarization, (3) a prolongation of the A. P. duration at 90% repolarization. During Ca++ excess perfusion the secondary depolarization is increased, shifted to more positive potentials and an earlier maximum value. It disappears during zero Ca++ and verapamil perfusion. Elevating the Ca++ concentration and shortening the pacing intervals before the period of rest increases the A. P. duration at 90% repolarization. Prolonging the pacing pause and decreasing the external Ca++ concentration delays the restitution of the steady state A. P. configuration after the rest By Ca++ excess the post rest A. P. restitution is accelerated. To explain the experimental findings, the possible role of a Ca++-sensitive K+ conductivity a poststimulatory variation of the slow inward current and the time-dependent K+ currents as well as processes of accumulation are discussed.

Action Potentials↗
PubMed1980

[Existence and properties of a chloride-sensitive conductivity in atrial myocardium].

Investigated are the intracellularly recorded action potentials (A. P.) of the rabbit atrial trabeculae (length 2-4 mm, diameter 150-800 micrometers). After a pacing pause the first A. P. shows a rapid initial repolarization (I. R.) up to -40 mV within 4-6 ms. By increasing the duration of the pacing pause the I. R. is accentuated. It is diminished by repetitive stimulation after the pause and disappears within 2-4 s. At variation of the extracellular Ca++ concentration and under verapamil, tetraethyl ammonium chloride load (TEA load) the I. R. is unchanged. On the other hand, the I. R. is very sensitive to the variation of the external Cl- concentration. When decreasing the external Cl- concentration, the I. R. is diminished. At 10 mmol x 1(-1) the I. R. disappears. Assuming a Cl- current ICl the experimental findings are modelled. During the A. P. a Cl- conductivity gCl is activated instantaneously and inactivated slowly (rate constant 5.09 s-1). Because of the repriming of gCl the I. R. disappears after the post rest pacing. During the pacing pause a recovery of gCl takes place (rate constant 0.06 s-1). The gCl recovery induces the post rest I. R. Estimation of the maximum gCl yields 0.24 mmho . cm-2.

Action Potentials↗
PubMed1980

[Effects of intracellular 4-aminopyridine and tetraethylammonium load on action potentials in the rabbit atrial myocardium].

Investigated are rabbit atrial trabeculae (2-4 mm length, 150-800 micrometers diameter). When using a standard microelectrode technique, the action potentials after an intracellular 4-AP and TEA load are prolonged. Only the TEA load significantly diminishes the resting potential of the beating preparations. The typical configuration of the action potential following a period of rest (rapid initial repolarization, secondary depolarization and a late retarded repolarization) is not changed qualitatively. During a repetitive stimulation after a pacing pause the action potentials' restitution is accelerated at 4-AP. After 4-AP and TEA load the secondary depolarization of the first post rest action potential is more accentuated. By reconstructing the post rest action potentials a 4-AP sensitive current is determined. At constant drive this current shows a threshold potential at -40 and a reversal potential at -10 mV. The current is inward directed between -40 and -10 mV and is outward directed at more positive potentials than -10 mV. After a pacing pause the current-voltage relation is shifted to more negative potentials. The 4-AP sensitive current is modelled by consideration of a slow activated (during the action potential) and deactivated (during the pacing pause) conductivity. Processes of accumulation are discussed.

4-Aminopyridine↗
PubMed1980

Rate-related changes of the transmembrane potential in the rabbit atrial myocardium.

We studied changes of the transmembrane resting and steady state action potentials in the rabbit atrial trabecular preparations (length 2-4 mm, diameter 150-800 micrometers, standard microelectrode techniques). Following cessation of rapid drive the transmembrane potential shows an initial depolarization and a terminal hyperpolarization. Increasing the stimulation frequencies before the cessation of driving the initial depolarization and the terminal hyperpolarization are more accentuated. When the stimulation frequency is abruptly reduced, the enddiastolic ("resting") potential increases (steady state resting potential - 82 +/- 3 mV at 1.0 s, -73 +/- 6 mV at 0.25 s driving interval). Decreasing the rate of stimulation the duration of the steady state action potential shortens at 25% and prolongs at 90% repolarization. A calculated background conductivity is diminished using a slower drive. From the experimental findings ensue some considerations about a K+ accumulation, the rate dependent sodium pump and the rate related shifts of the steady state outward current-voltage relationships.

Action Potentials↗
PubMed1979

The influence of prostaglandins E2 and F2 alpha on electrotropic and inotropic vagal effects on the isolated rabbit atrium.

1. PG E2 (2.10(-8) g/ml) produces a positive inotropic effect and lengthens the duration of the action potential at the level of 50% and 90% of repolarization. 2. PG F2 alpha acts negatively inotropic and shortens the action potential at the level of 75% and 90% of repolarization. 3. PG F2 alpha (2.10(-8) g/ml) increases both the electrotropic and inotropic vagal effects, PG E2 (2.10(-8) g/ml) decreases them. 4. PG E2 improves the electromechanical coupling, PG F2 alpha reduces it.

Action Potentials↗