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Biomedical subjects

B Nilius

Publications and source records attributed to B Nilius.

251 records · Page 14Linked to original sources
PubMed1979

[Membrane current and Ca++-transport during the action potential of the rabbit atrium changed by acetylcholine and extracellular Ca++-concentration].

Using a modified sucrose gap technique action potential and phase plane trajectories of trabeculae from the left rabbit's auricle were recorded. By means of a numerical treatment and some mathematical model interpretations from these measurements current-voltage-(I-V)-relationships and the amount of inward transported calcium are calculated. A time independent K+-current shows that a voltage region within the anomalous rectification should exist. By acetylcholine the anomalous rectification is abolished and the inward transported amount of Ca-ions by the action potential (Q) decreases. A conductance of the K+-current gK will be dimished by decreasing the extracellular calcium concentration. The amount of inward transported calcium does not change significantly by variation of the extracellular calcium concentration. The calcium amount Q should contribute 17% of the calcium necessary for maximum contraction.

Acetylcholine↗
PubMed1979

[Effect of cesium ions on the electrotropic actions of acetylcholine in the rabbit atrium].

Cs+ (15-20 mM) decreases the electrotropic vagal effects on an isolated vagal innervated rabbit atrium. By means of investigating the action potentials and the phase plane trajectories of trabeculae from the rabbit atrium using a modified single sucrose gap technique the anomalous rectification disappears and also the effect of acetylcholine (ACh) on action potential duration. We presume that the anomalous rectification should be a necessary condition of electrotropic vagal (ACh) action on the rabbit atrium.

Acetylcholine↗
PubMed1979

[Action of acetylcholine on the mammalian auricle influenced by verapamil].

The action of acetylcholine (ACh) and verapamil (VePa) on the action potential (V(t)), phase plane trajectories of V(t) (dV/dt--V(t) -- plot) and isotonic contractions were investigated using an isolated vegal innervated preparation from rabbit atrium (method I) and investigating action potentials from atrial trabeculae by means a modified sucrose gap technique (method II). If the VePa-concentration increases to 4 mg/1 the duration of the action potential decreases at 20 and 90% repolarization (driving frequencies 2 s-1). In the VePa-solutions phase plane trajectories of the action potential did not change significantly. ACh application favours the disappearance of a region in the repolarization phase plane plot showing anomalous rectification (d(--dV/dt)/dV less than 0) both by control conditions and verapamil. The electrotropic ACh-and vagal effects will be unchanged by verapamil. The inotropic ACh-and vegal action (method I) increases by VePa (2 mg/1). The action of ACh and verapamil will be analysed using a mathematical model for reconstructing the repolarization phase of mammalian atrial myocardium action potentials.

Acetylcholine↗
PubMed1979

[Electrotropic acetylcholine action on the mammalian auricle by means of the "phase plane" trajectories of the action potential].

A single sucrose gap techniques has been used to study action potentials and phase plane trajectories of them in atrial trabeculae of the rabbit. Using polynomial representations of current-voltage relationships a model of membrane action potential of atrial myocardial fibres is described and allows an interpretation of recording data from the phase plane trajectories. Our findings show: 1. Increasing extracellular calcium concentration increases a potassium conductivity of the atrial membrane. 2. An anomalous rectification concerning repolarizing currents in atrial fibres decreases with increasing extracellular calcium. 3. Acetylcholine (3.10(-4) g.cm-3) abolishes the anomalous rectification. These results are discussed in relation to previous electrophysiological studies of negative electrotropic effects of acetylcholine in cardiac muscle.

Acetylcholine↗
PubMed1979

[Quantitative description of a calcium induced potassium conductance of the rabbit atrial myocardium by variation of the Ca++ concentration].

Action potentials of trabeculae from the left rabbit atrium were studied using a modified sucrose gap method. A mathematical treatment of the action potential time course and the phase plane trajectories gives an approximation of a potassium conductance of gK.GK increases be action potential shows a maximum at 1 s.gK reaches a steady state level after 40 s. The experimental findings are interpreted by means a mathematical model of a Ca++-induced K+-conductance.

Action Potentials↗
PubMed1978

Modelling of hypertrophic heart potentiation with reference to morphological measurements.

Potentiation of heart muscle stripes of the right ventricle was investigated in normal rats (NT-group) and in rats stressed by swimming (HT-group). The mean fibre diameter runs to 26 micrometer in HT-group and 16 micrometer in NT-group. The difference was significantly high, as well as that of relative heart weights. The potentiation by paired pulse stimulation was more marked in HT-group than in NT-group. The interval-strength-relationships increase with prolongation of the driving interval. Potentiation is greater in loaded rats than in normal rats. A mathematical model for Ca++-storage in sarcoplasmic reticulum is introduced. Decrease of basic-filling of Ca++-store is modelled to HT-group with support of morphological measurements and is discussed as reason for improved properties of potentiation of HT-group.

Action Potentials↗
PubMed1978

[Properties of vagal excitation transfer to the heart atrium].

A mathematical model of pre- and postganglionic parasympathetic nerve fiber excitation transfer is developed. This model gives a measure Q of acetylcholine (ACh) release from presynaptic preganglionic boutons and postganglionic varicosities. When increasing Ca++ the measure Q increases too. Na-ions exert a competitive inhibition. The relationship between Q and the Ca/Na2-quotient is a hyperbolic one. Mn++ inhibits the release of ACh non-competitively. Q increases both by excess potassium and Cs+ depolarization. The ACh release is diminished by Mg++. Ba++ cannot replace the effect of Ca++ on ACh release in Ca++ depleting conditions. Q increases with decreasing pH-level. The ACh release is not significantly influenced by increasing pH, Verapamil (4 mg/l), prostaglandins E2 and F2alpha (20 ng/ml) and substitution of nonpermeable anions for Cl-.

Acetylcholine↗
PubMed1977

[Modification of efferent vagal effects on the isolated atrium by increased extracellular K+ concentrations].

Isolated vagal-innervated rabbit atria are electrically driven. Alterations of action potential, contraction, and electrotropic and inotropic vagal effects are investigated during variations of the external potassium concentration. Action potential area and contraction amplitude decrease by increasing external potassium concentration. If the potassium concentration is higher than 11 mM, the action potential disappears. At 24 mM potassium concentration the contraction amplitude of the driven atrium is reduced to 2%. Adrenaline (2.10(-5) g/ml) causes a restitution of the action potential and the contraction. With increasing potassium concentration the inotropic and the electrotropic vagal effectivity increases also. The vagal effects at the adrenaline restituted action potentials and contractions (15 mM potassium, 2.10(-5) g/ml adrenaline) are also higher than in normal solutions. The relations of electromechanical coupling are altered by potassium variation at the same coupling curve. With increasing potassium concentration the reproducibility of the vagal effects decreases.

Action Potentials↗
PubMed1977

[Relationship of inotropic vagal effects to stretching of the atrium].

Isolated left rabbit atria were tested. Preparations are vagal innervated and driven by a constant frequency. Isovolumetric contractions, volumes of the auricles and intraatrial pressures were recorded. With increasing intraatrial pressure the effectivity of peripheral nerve-ending stimulation decreases. There exists a critical value of atrial area. The vagal effectivity will decrease rapidly, if the atrial surface increases higher than this critical value by stretching the auricles.

Animals↗
PubMed1977

[The effect of Mn++ on the electrotropic and inotropic vagal effect].

An isolated rabbit atrium, innervated by vagal nerve, was tested. Increased Mn++ concentrations decrease the areas of the action potentials and the amplitudes of contractions. At 2 mM Mn++ the contraction disappears and an extremely sharp action potential is recorded. By variation of both Ca++ and Mn++ concentrations one can observe parallely shifted concentration-response curves for the amplitudes of the contractions. This result is described by the model of a competitive-antagonistic Mn++-Ca++ action. At 1 mM Mn++ the inotropic and electrotropic effects disappear. Small concentrations of Mn++ (0.15 mM) increase the electrotropic vagal effects. At 0.5 mM Mn++ both vagal effects are diminished. The discussion of the results is based on the action of acetylcholine on the slow inward current of calcium and sodium ions.

Animals↗
PubMed1976

[Effects of hypertrophy on the behavior of potentials in isolated ventricular strips of the rat].

Potentiation of right-ventricular strips obtained from normal rats (NT-group) and from rats showing hypertrophic hearts as a result of long-time swimming (HT-group) has been investigated. Strength-interval relationships, poststimulation potentiation and the potentiation by paired stimulation has been tested. The behavior of the action potential in both groups showed no significant differences. Standardized strength-interval relationships of HT-group were steeper than those of the NT-group. Maximal potentiation in the HT-group occurred at shorter delay-intervals. Potentiation after long-time pauses was greater in the HT-group. The results are discussed on the basis of model considerations of electro-mechanical coupling.

Action Potentials↗
PubMed1975

[Adaptation of electropic and ionotropic vagal effects on the isolated rabbit atrium].

Long-time vagal stimulation induces a decrease of electrotropic and inotropic effects on the isolated rabbit atrium in spite of constant stimulation frequency. This decrease is defined as effect adaptation. To compensate this effect adaptation, the n. vagus was stimulated with increasing stimulation frequency. Compensation is possible for a certain period referred to as control time. The adaptation of the electrotropic effects is more delayed and weaker than the inotropic effect adaptation. The control times of the electrotropic effect are longer than those of the inotropic effect. Acetylcholine perfusion without vagal stimulation shows the same results. It was shown that the effect adaptaion does not result from depletion of acetylcholine stores or from co-stimulation of sympathetic nerve fibres. The effect adaptation is discussed as being the result of machano-electrical coupling.

Acetylcholine↗
PubMed1975

[Quantitative description of the adaptation of vagal effects by means of an electromechanical coupling model].

A four compartments model describes the electrotropic and the inotropic vagal effect time courses during long time stimulation. The model realises electro-mechanical coupling. A differential equation for the coupling model is developed, solutions are given and a numerical treatment is described. The model shows the essential properties of effect adaptation: time delay and smaller extent of electrotropic effect adaptation.

Action Potentials↗
PubMedDate not supplied

A novel type of cardiac calcium channel in ventricular cells.

Calcium influx is vital for several aspects of cardiac activity, so it is important to ask if heart cells possess a single or multiple types of Ca channel. Only one Ca channel type has been identified in patch-clamp studies of unitary current, despite suggestions to the contrary from whole-cell recordings in heart cells and unitary recordings from other cells. Here we describe a novel type of cardiac Ca channel with several properties that distinguish it from the hitherto-identified Ca channel in heart cells. Its conductance in isotonic Ba is small (8 pS), and is no larger in Ba than in Ca. It activates and inactivates at relatively negative potentials and remains functional long after patch excision. It is insensitive to dihydropyridines such as nimodipine and the Ca agonist Bay K 8644, and is more resistant to block by external Cd than the previously described type of cardiac Ca channel.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMedDate not supplied

Multiple types of chloride channels in bovine pulmonary artery endothelial cells.

We have characterized two different types of Cl- currents in calf pulmonary artery endothelial (CPAE) cells by using a combined patch-clamp and Fura-2 microfluorescence technique to measure simultaneously ionic currents and the intracellular Ca2+ concentration, [Ca2+]i. Exposure of CPAE cells to 28% hypotonic solution induces cell swelling without a change in membrane capacitance and [Ca2+]i, and concomitantly activates a current. This current, I(Cl, vol), is closely correlated with the changes in cell volume and shows a modest outward rectification. It slowly inactivates at potentials more positive than +60 mV but is time- and voltage-independent at other potentials. Increase in [Ca2+]i by different maneuvers, such as application of vasoactive agonists (ATP), ionomycin, or loading of the cells directly with Ca2+ also activates a Cl- current, I(Cl, Ca). This current slowly activates at positive potentials, inactivates quickly at negative potentials and shows strong outward rectification. A time-independent component of the current activated by elevation of [Ca2+]i alone can be inhibited by cell shrinking by exposing the cells to hypertonic solution, indicating that an increase in [Ca2+]i also co-activates I(Cl, vol). Forskolin or cAMP never activated a current in CPAE cells, which indicates the lack of cAMP-activated channels in these cells. There is also no evidence for the existence of voltage-gated Cl- channels in resting, nonstimulated cells. Challenging a cell with elevated [Ca2+]i and hypotonic solutions activated I(Cl, vol) on top of I(Cl, Ca), suggesting that I(Cl, Ca) and I(Cl, vol) are different channels. We conclude that CPAE cells do not express voltage-gated (ClC-type) or cAMP-gated (CFTR-type) Cl- channels, but activate large Cl- currents after volume (mechanical?) or chemical (Ca2+) stimulation.

Animals↗