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H Reuter

Publications and source records attributed to H Reuter.

At least 181 records · Page 10Linked to original sources
PubMed1970

Voltage clamp experiments on ventricular myocarial fibres.

1. A voltage clamp method utilizing a sucrose gap and glass microelectrodes was developed and used to study dog ventricular myocardial fibre bundles. The limitations and the reliability of this method are demonstrated by a series of tests.2. A dynamic sodium current, excited at membrane potentials more positive than -65 mV, was measured. The equilibrium potential for this large, rapid inward current depends directly on [Na](o), shifting 29.0 +/- 2.3 mV (+/- S.E. of mean), as opposed to a theoretically expected value of 30.6 mV, when [Na](o) is reduced to 31% of normal.3. Sodium current is inactivated by conditioning depolarizations. Complete inactivation occurs with conditioning potentials more positive than -45 mV, and 50% inactivation occurs at about -55 mV. The location of the inactivation curve shifts along the voltage axis, when [Ca](o) is varied between 0.2 and 7.2 mM.4. A second, much smaller and slower net inward current, with a threshold around -30 mV, and an equilibrium potential above +40 mV was also observed.5. The ;steady-state' current-voltage relationship (after 300-600 msec) exhibits inward-going (anomalous) rectification with negative slope between -50 and -25 mV.6. A small, very slowly developing component of outward current was observed at inside positive potentials. The equilibrium potential for this current, although slightly dependent on [K](o), is neither identical with the potassium equilibrium potential nor with the resting potential in normal Tyrode solution.7. Anatomical limitations, primarily resistance in the extracellular space within the bundle, prevent complete characterization of the rapid, large sodium current, but do not limit the application of the clamp method to the study of other, smaller and slower currents. The evidence for this is discussed extensively in the Appendix.

Animals↗
PubMed1970

Membrane calcium current in ventricular myocardial fibres.

1. A slow inward current in ventricular preparations of the dog heart can be measured by the voltage clamp method without interference from the initial rapid sodium current if the sodium system is inactivated by conditioning depolarization.2. The slow inward current is very sensitive to variation in [Ca](o). It occurs above the equilibrium potential of I(Na) immediately after changing the bathing fluid to a sodium-free solution and persists under this condition for a long time without much alteration, while I(Na) is rapidly abolished. Tetrodotoxin and [Mg](o) have no effect on this current component. These results strongly support the view that the slow inward current in cardiac tissue is carried by calcium ions.3. The threshold for initiation of the calcium current is around -35 mV in Tyrode solution and is shifted to more negative potentials by either increasing [Ca](o) or reducing [Na](o).4. Calcium sensitive inward current tails associated with repolarization are assumed to represent a proportional measure of calcium conductance activated during the preceding depolarization. Calcium conductance declines rapidly with time in the inside negative potential range and slowly at positive potentials. The time constants for this ;inactivation' process vary between 40 and 700 msec in the potential range -35 to +50 mV.5. By using instantaneous current-voltage relations the reversal potential of calcium current was estimated to be about +60 mV in normal Tyrode solution. As shown in the Appendix, however, the calcium equilibrium potential cannot be considered to be constant.6. The importance of the calcium current for the plateau of the cardiac action potential is discussed.

Animals↗
PubMed1970

The relation between membrane potential, membrane currents and activation of contraction in ventricular myocardial fibres.

1. Membrane currents and contractile responses have been measured in ventricular myocardial preparations under voltage clamp conditions.2. In Tyrode solution, steady-state contraction was obtained only after 5-8 depolarizations to a given potential level. The threshold of steady-state tension was identical to the potential where the calcium inward current, I(Ca), was activated (about -35 mV). Both thresholds were shifted in the same direction along the voltage axis and by the same amount by changing [Ca](o) or [Na](o). Maximum tension was obtained at inside positive potentials.3. The time courses of steady-state tension and of activation of I(Ca) were different by more than one order of magnitude in Tyrode solution. But in order to achieve any appreciable steady-state tension, I(Ca) had to flow during several identical depolarizations. Tension decreased again at potentials above E(Ca). This suggests that calcium inward current must flow in order to fill intracellular calcium stores from which calcium can be released by an unknown mechanism.4. The ability of a fibre bundle to contract again after a preceding twitch is greatly dependent on the membrane potential between two equal depolarizations. In Tyrode solutions with 1.8 and 7.2 mM-CaCl(2) half restoration of this ability occurred at -45 +/- 3 mV (+/- S.E. of mean) and -23 +/- 4 mV, respectively.5. In sodium-free bathing solutions, steady-state tension was attained upon the first depolarization provided I(Ca) was activated. Furthermore, at different potentials, the time courses of activation of tension and of activation of I(Ca) were identical, i.e. tension reached its maximum when I(Ca) was fully activated. This suggests that in sodium-free solutions the flow of calcium ions into the fibre directly activates contraction.

Animals↗
PubMed1970

The effect of the internal sodium concentration on calcium fluxes in isolated guinea-pig auricles.

1. Calcium efflux from guinea-pig auricles followed saturation kinetics when [Ca](o) and [Na](o) were changed while the ratio [Ca](o)/[Na](o) (2) was kept constant. The Michaelis constant, K(m) (Ca+Na) = 40 mM, suggests that a hypothetical carrier system, responsible for sodium-calcium exchange, is far from saturation with the inside concentrations of these ions.2. [Na](i) was altered in the auricles between 12.5 and 60 mM/kg fibre water while total cellular calcium concentration ([Ca](t)) at the beginning of the influx period was not significantly different in the various groups of preparations.3. (45)Ca influx increased appreciably with increasing [Na](i). (45)Ca influx from sodium-poor solution corresponded to an almost equal increase in [Ca](t), while [Ca](t) did not change much in preparations loaded with (45)Ca in Tyrode solution. When the sodium-activated fraction of calcium influx was plotted against [Na](i) (2) the resulting curve indicated saturation with K(m) (Na) = 3500 (mM [Na](i))(2) and maximal influx rate, J(i, max) (Ca') = 1.35 mM/kg wet weight x 10 min.4. When the preparations were re-equilibrated for various times in normal Tyrode solution after [Na](i) had been increased, both the sodium-activated component of calcium influx and [Na](i) (2) decreased with approximately the same rate constants.5. Calcium efflux from auricles with high [Na](i) was increased when it was measured in Tyrode solution while the efflux in sodium-poor solution was inhibited.6. Auricles with increased [Na](i) showed a positive inotropic contractile response.7. The main conclusion reached by these experiments is that calcium influx is affected by [Na](i) in a way which is compatible with a carrier-mediated sodium-calcium exchange system.

Animals↗