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S L Lipsius

Publications and source records attributed to S L Lipsius.

43 records · Page 3Linked to original sources
PubMed1982

Acetylcholine and potassium-42 movements in right atrial muscle of the guinea pig.

The effect of acetylcholine (ACh) on potassium (K-42) movements has been studied in right atrial tissue of the guinea pig. When quiescent fibers were stimulated at 108 beats/min, potassium uptake was increased to a small but significant extent. Administration of acetylcholine (2.7 X 10(-6) M) induced an increase in potassium uptake that was greater in fibers that were quiescent than in the same fibers when stimulated. The ACh induced increase in potassium uptake was abolished by atropine (5.2 X 10(-7) M) and enhanced in the presence of nicotine (10(-5) M). In addition, ACh induced an increase in potassium efflux that was greater in fibers that were quiescent than in the same fibers when stimulated. Atropine blocked the effect of ACh on potassium efflux. It is concluded that activity of atrial tissue increases potassium uptake and modifies the action of ACh on potassium uptake and efflux. Muscarinic receptors mediate the ACh induced increase in potassium movements. Nicotinic receptors may mediate an ACh induced decrease in potassium uptake in atrial muscle.

Acetylcholine↗
PubMed1982

Voltage and time dependence of restitution in heart.

Between beats, cardiac muscle gradually recovers the ability to contract in response to a stimulus. We examined the time and voltage dependence of this "restitution" process using sheep cardiac Purkinje fibers that were voltage clamped by the two-micro-electrode technique. The rate and time course of restitution depended on the voltage and duration of preceding conditioning depolarizations. As the voltage of a conditioning depolarization was made less negative, the early rate of restitution increased, the process reached a greater peak value, and oscillations in the time course of restitution became more likely. When conditioning depolarizations were to voltages near or above the normal action potential plateau, increasing their duration had much the same effect as increasing voltage. However, with conditioning depolarizations to -40 or -50 mV, prolongation had little or no effect on the subsequent rate of restitution. The voltage during restitution affected both the time course and final extent of restitution. Steady-state restitution was an approximately sigmoid function of voltage. The early rate and peak value of restitution increased as the voltage during restitution was made more negative. Oscillations of restitution were dramatic at voltages between -70 and -50 mV. The behavior of restitution confirms that most of the calcium that activates contraction comes from intracellular stores. The complex time and voltage dependence of restitution suggests that the process reflects the time course of calcium reaccumulation in an internal store.

Animals↗
PubMed1982

Membrane currents, contractions, and aftercontractions in cardiac Purkinje fibers.

We examined relationships between isometric tension and membrane currents in sheep Purkinje fibers voltage clamped by the two-microelectrode method. Oscillatory restitution of contractility was accompanied by a small oscillation in membrane current and by an aftercontraction. The membrane current oscillation resembled the transient inward current (TI) others have reported in the presence of strophanthidin. Twitches produced by voltage clamp depolarizations did not correlate with net outward current in normal solution, but when the early outward current was blocked by 0.5 mM 4-aminopyridine, the residual outward current did correlate with twitches elicited by strong depolarizing clamps, particularly in solutions containing higher than normal calcium concentrations. The results illustrate important similarities and differences between membrane current behavior in sheep Purkinje fibers and behavior others have reported in calf fibers. Correlations between restitution, aftercontractions, and TI's, and between twitch tension and a component of outward current, may arise because of calcium regulation of membrane conductance, electrogenic Na-Ca exchange, or a combination of these and other mechanisms.

4-Aminopyridine↗
PubMed1980

Acetylcholine lengthens action potentials of sheep cardiac Purkinje fibers.

The effect of acetylcholine (ACh) on the electrical activity of sheep cardiac Purkinje fibers was studied using standard microelectrode techniques. Most fibers showed a definite sequence of changes when exposed to ACh. Initially, action potential duration (APD) increased markedly. After about 20 s, the maximum diastolic potential (MDP) started to become more negative and, at the same time, the rate of increase in APD slowed. Once the MDP stabilized at a more negative level, the APD usually resumed its rapid increase. ACh also increased the slope of diastolic depolarization and made the plateau voltage more positive. APD was increased by ACh concentrations as low as 10(-7) M, and it increased with concentrations up to 10(-5) M (the highest concentration tested). ACh-induced increases in APD depended on the stimulation frequency; 2-min exposures to 10(-6) M ACh increased APD by 76.8 +/- 14.7% at 6 min-1 and 17.7 +/- 4.2% at 60 min-1. Atropine blocked all the effects of ACh. Hexamethonium did not prevent the ACh effects. It is concluded that ACh acts via muscarinic receptors. The changes in APD and MDP appear to be separate events, and it is difficult to see how the former effect may be explained by known actions of ACh.

Acetylcholine↗
PubMed1977

Acetylcholine-norepinephrine interactions on potassium movements in the sinus node.

Possible adrenergic mechanisms involved in acetylcholine (ACh) induced potassium movements in the sinus node have been investigated using a tracer potassium (42K) and a microelectrode technique. The ACh-induced increase in 42K uptake was enhanced by propranolol and was unaffected by phentolamine. Reserpinization neither prevented the ACh-induced increase in 42K uptake nor the enhanced effect in the presence of propranolol. In reserpinized preparations, ACh-induced 42K uptake was the same before and after norepinephrine (NE) administration, but was greater after acute reserpinization. NE alone induced an increase in 42K uptake but the simultaneous administration of ACh and NE provoked an increase in 42K uptake similar to that obtained with ACh alone. When both neuromediators and atropine were given simultaneously, an increase in 42K uptake did not occur. Thus, the ACh induces an increase in 42K uptake independently of NE. ACh antagonizes the NE effect on 42K uptake independently of a muscarinic interaction.

Acetylcholine↗
PubMed1977

Effects of acetylcholine on potassium movements in the guinea-pig sinus node.

Factors influencing the effect of acetylcholine (ACh) on potassium movements in the sinus node have been studied using tracer potassium (42K) and a microelectrode technique. The following results were obtained. ACh has qualitatively different effects on 42K uptake depending upon concentration, i.e., small concentrations (approximately equal to 10(-9) M) of ACh may decrease and larger concentrations (greater than or equal to 10(-7) M) increase 42K uptake. The ACh induced increase in 42K uptake is slightly but significantly greater when the rate of discharge is maintained constant by electrical drive than when the rate is slowed by ACh as quantitated by transmembrane recordings. In the presence of atropine, the ACh-induced increase in 42K uptake is abolished and replaced by a small but consistent decrease. Blockage by nicotine enhances the ACh-induced increase in 42K uptake and blockade by d-tubocurarine diminishes it. The effect of ACh on 42K uptake is greater in high (5.4 mM) than in low (0.54 mM) [Ca]0. These results suggest the conclusion that ACh acts upon a muscarinic recpetor to increase and on a nicotinic receptor to decrease potassium uptake. The net effect depends upon the concentration of ACh. The action of ACh on potassium uptake is modulated by [Ca]0.

Acetylcholine↗