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H Reuter

Publications and source records attributed to H Reuter.

At least 145 records · Page 8Linked to original sources
PubMed1975

The effect of substances releasing intracellular calcium ions on sodium-dependent calcium efflux from guinea-pig auricles.

1. 45-Ca efflux and resting tension were measured in isolated guinea-pig auricles under conditions known to change the intracellular free Ca ion concentration. 2. In the presence of [Na]o, caffeine (2mM) increases 45-Ca efflux, but does not produce a contracture, while in the absence of [Na]o and [Ca]o caffeine causes a contracture without increasing 45-Ca efflux. Adrenaline (10-minus5-10-minus 4M) with or without theophylline (0-5-1-0mM) has no effect on either 45-Ca efflux or resting tension. 3. In the presence of caffeine the rate of net efflux of Ca depends on [Na]o-2. Caffeine contractures of muscles in Na-free solution relax upon the addition of [Na]o. Relaxation is correlated with the increase in net efflux of Ca. 4. Cyanide (2mM) produces a variable increase in 45-Ca efflux without a concomitant contracture in Na-containing solutions, but in Na, Ca-free solutions a large contracture occurs without significant increase in 45-Ca efflux. 5. A large increase in 45-Ca efflux and a contracture were observed with the 'Ca-ionophore' X 537 A. 6. Changes in membrane potential (K-depolarization) in hypertonic solutions have no significant effect on Na-dependent 45-Ca efflux, which is an agreement with an electroneutral 2:1 Na-Ca exchange. 7. Cyanide and X 537 A both cause a considerable release of Ca ions from isolated guinea-pig heart mitochondria, while caffeine has no effect. 8. The results suggest a powerful role of the Na-Ca exchange system in reducing the intracellular Ca concentration after Ca release from intracellular stores.

Animals↗
PubMed1975

Inward calcium current and activation of contraction in mammalian myocardial fibers.

Electrophysiological and tracer studies show an increase in Ca permeability of cardiac cell membranes during excitation. The Ca influx (ICa) during the plateau of the cardiac action potential is a voltage- and time-dependent electrogenic process. The following results were obtained by simultaneous recordings of twitch tension (T) and membrane ionic currents under voltage clamp conditions. 1) The threshold potentials for T and ICa are the same. 2) T decreases when the reversal potential by ICa is approached during depolarization. 3) The voltage and time dependences of recovery of ICa and of T from inactivation are very similar. 4) Catecholamines and methylxanthines which exert a positive inotropic effect increase ICa. 5) Substances which reduce ICa (La3+, Co2+, Mn2+, verapamil, and D 600) cause a negative inotropic effect. Despite these parallelisms the relation between ICa and T is indirect since during repetitive identical depolarizations ICa decreases while T increases (staircase). This can be explained by a store (sarcoplasmic reticulum?) into which Ca ions flow and from which they are released. Other factors like Na-Ca exchange influence the filling of these stores.

Action Potentials↗
PubMed1975

[Action potentials and ionic currents].

Our knowledge of the ionic currents underlying the cardiac action potential has much increased in recent years. Principally three membrane current components are characterised, of which the change carries are sodium ions, calcium ions and potassium ions. Different drugs influence the current components in various ways. For an extensive description of the ionic currents in the heart, the bibliography is given.

Action Potentials↗
PubMed1974

[Pyrithioxin].

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Adolescent↗
PubMed1974

Slow recovery from inactivation of inward currents in mammalian myocardial fibres.

1. Reactivation kinetics of the rapid and slow inward currents in ventricular fibres have been assessed by studying the maximum rate of rise ((dV/dt)max) of the action potential upstroke and the duration of the plateau in progressively earlier premature responses. Reactivation of the slow inward current was also studied by voltage clamp technique in sheep and pig ventricular trabeculae.2. The time constant of recovery of (dV/dt)max was voltage dependent and increased from less than 20 msec when the resting membrane potential was more negative than -80 mV to more than 100 msec when the resting membrane potential was between -65 and -60 mV. Similar results were obtained in Purkinje fibres. These results suggest that the time constant for reactivation is slower than the time constant for inactivation of the rapid inward current system by at least one order of magnitude.3. The time constant of recovery of plateau duration was also voltage dependent and increased from 30 to 70 msec as the membrane potential was changed from -85 to -60 mV.4. The reactivation time constant of the slow inward current determined by voltage clamp experiments were similar to the results obtained by analysis of plateau duration. At potentials less negative than -60 mV the time constant of reactivation became progressively longer. Unlike reactivation time constants of (dV/dt)max, the time constants of reactivation of the slow inward current were similar to the time constants of inactivation.5. Our results indicate that (a) in premature action potentials, time as well as voltage are important determinants of (dV/dt)max in myocardial and Purkinje fibres, (b) the kinetics of reactivation of the rapid inward current in cardiac fibres are different from those in nerve and (c) plateau duration of premature action potentials in ventricular myocardial fibres is largely determined by the kinetics of reactivation of the slow calcium inward current.

Action Potentials↗
PubMed1974

Localization of beta adrenergic receptors, and effects of noradrenaline and cyclic nucleotides on action potentials, ionic currents and tension in mammalian cardiac muscle.

1. Isoprenaline and noradrenaline were applied iontophoretically to cardiac Purkinje fibres. Intracellular application of the drugs had no effect, while extracellular application of the same amounts of charge caused acceleration of pace-maker activity and a shift of the plateau level of the action potential. These results indicate that beta-adrenergic receptors are located at the outside of the cardiac cell membrane.2. A systematic comparison of the effects of cyclic AMP derivatives and noradrenaline on action potentials and isometric tension of ventricular myocardial preparations showed that the nucleotides and the catecholamine increase the plateau height and the duration of the action potential and also increase tension. However, there are quantitative differences in the action of these drugs.3. Cyclic AMP derivatives and noradrenaline increase the slow inward current, I(Ca), in ventricular myocardial preparations. Voltage clamp analysis of I(Ca) showed that the kinetic parameters of this membrane current are not affected by these drugs. However, the membrane conductance to Ca ions is greatly increased by noradrenaline and to a smaller extent by dibutyryl cyclic AMP.4. Concentration-response relations of the membrane effects of noradrenaline on plateau height of the action potential and on I(Ca) could be fitted by the same theoretical log concentration-response curve. The Hill plot of this concentration-response curve had a slope of 2. The half maximal response occurred at 5 x 10(-7)M.5. The results are compared with other membrane effects of catecholamines and cyclic nucleotides in cardiac muscle. The effects on I(Ca) are related to the positive inotropic effect of the drugs.

Action Potentials↗