Influence of streptomycin on spontaneous activity of clusters of cultured cardiac cells from neonatal rats

1980 ◽  
Vol 58 (4) ◽  
pp. 433-435 ◽  
Author(s):  
M. D. Payet ◽  
G. Bkaily ◽  
O. F. Schanne ◽  
E. Ruiz-Ceretti
Keyword(s):  
Action Potential ◽  
Action Potentials ◽  
Maximum Rate ◽  
Cardiac Cells ◽  
Neonatal Rats ◽  
Slow Response ◽  
Diastolic Depolarization ◽  
Beating Rate ◽  
Maximum Rate Of Rise ◽  
Diastolic Potential

In clusters of trypsinized ventricle cells from neonatal rats which exhibit slow response action potentials, streptomycin in concentrations from 0.17 to 5.5 mM significantly inhibits the beating rate. Microelectrode experiments performed at a concentration of 5.5 mM revealed a reduction in the slope of diastolic depolarization from 149 to 53 mV/s whereas the maximum diastolic potential depolarized from −42.4 to −33.6 mV which entailed a decrease in overshoot and maximum rate of rise of the action potential. We conclude that the decrease of the slope of diastolic depolarization mainly determines the slowing of the beating rate and that streptomycin interferes with the pacemaker mechanism usually associated with the slow response.

Prolongation and shortening of action potentials by electrical shocks in frog ventricular muscle

1994 ◽  
Vol 266 (6) ◽  
pp. H2348-H2358 ◽  
Author(s):  
S. B. Knisley ◽  
W. M. Smith ◽  
R. E. Ideker
Keyword(s):  
Action Potential ◽  
Action Potentials ◽  
Maximum Rate ◽  
Transmembrane Potential ◽  
Ventricular Muscle ◽  
Intracellular Action Potential ◽  
Electrical Shocks ◽  
Intracellular Action ◽  
Maximum Rate Of Rise ◽  
Diastolic Potential

Effects of electrical shocks on myocardium are important for defibrillation. We measured effects of shocks (5 ms, 1–40 V/cm) in isolated frog ventricular strips. We recorded contraction strength and intracellular action potential (AP) with a shock-voltage cancellation technique to allow recordings immediately after shocks. Shocks of > or = 5 V/cm produced a dose- and latency-dependent prolongation of the AP ongoing during the shock. Stronger shocks of 28–40 V/cm decreased the duration, maximum diastolic potential, amplitude, and maximum rate of rise of the phase zero depolarization of paced APs that began after the shock. The contraction strength increased 43 and 59% during the 10 s after the stronger shocks. The transmembrane potential was shifted toward 0 mV immediately after the stronger shocks. We concluded that weak or strong shocks prolong the AP ongoing during the shock, whereas sufficiently strong shocks also shorten APs that begin after the shock. AP prolongation and shortening may be important for defibrillation and acceleration of tachycardia after failed cardioversion shocks.

Effects of K-channel blockers, calcium, and verapamil suggest different pacemaker mechanisms in cultured neonatal rat and embryonic chick ventricle cells

1989 ◽  
Vol 67 (7) ◽  
pp. 795-800 ◽  
Author(s):  
Otto F. Schanne ◽  
L. Boutin ◽  
J. Derosiers
Keyword(s):  
Cardiac Cells ◽  
Neonatal Rat ◽  
K Channel ◽  
Chronotropic Effect ◽  
Inward Current ◽  
Diastolic Depolarization ◽  
K Current ◽  
Beating Rate ◽  
Rat Ventricle ◽  
Diastolic Potential

We compared the determinants of spontaneous activity in explanted neonatal (2-day-old) rat ventricle cells and in reaggregates derived from 15-day-old chick embryos. We studied the beating rate with an optical recording method and the underlying electrical activity with glass microelectrodes using the K current blockers cesium (Cs) and tetraethylammonium, varied Ca concentrations, and the Ca antagonist verapamil. In the rat (i) Cs increased the beating rate that was mediated by an increase in the slope of the diastolic potential, (ii) Ca increased the beating rate dramatically at low and medium concentrations to decrease it again at 8 mM Cao.2This increase in the beating rate was mediated by an increase of the slope of the diastolic depolarization. (iii) The beating rate decreased with verapamil at concentrations between 0.5 and 2.0 μM. The effects of Cs and Ca suggest that an increase in net inward current (block of IK1) underlies the positive chronotropic effect of Cs and that the pacemaker mechanism is determined by a Ca inward current or an IT1 type current modulated by variations of Cai. In the chick reaggregates (i) Cs and tetraethylammonium decreased the beating rate that was mainly brought about by a decrease in the slope of diastolic depolarization. (ii) Ca increased the beating rate but to a lesser degree than in the rat and there was no decrease of the beating rate at higher concentrations. (iii) The increase in the beating rate was not mediated by an increase in the slope of the diastolic potential but mainly by a depolarization of the maximum diastolic potential. (iv) Verapamil inhibited electrogenesis before any change in the diastolic potential was evident. The negative chronotropic effect of Cs and tetraethylammonium is compatible with the notion that a voltage- and time-dependent K current was inhibited and that this current determines the pacemaker. Moreover, the Ca component of the pacemaker mechanism in explanted rat ventricle cells resembles either that of the sinoatrial node or represents triggered activity.Key words: pacemaker mechanism, cultured cardiac cells, K-channel blocker, calcium, verapamil.

Calcium action potentials in single freshly isolated smooth muscle cells

1980 ◽  
Vol 239 (5) ◽  
pp. C162-C174 ◽  
Author(s):  
J. V. Walsh ◽  
J. J. Singer
Keyword(s):  
Smooth Muscle ◽  
Action Potential ◽  
Smooth Muscle Cells ◽  
Action Potentials ◽  
Maximum Rate ◽  
Muscle Cells ◽  
Membrane Resistance ◽  
Inward Current ◽  
Visceral Smooth Muscle ◽  
Maximum Rate Of Rise

The ionic basis of the action potential was investigated using intracellular microelectrodes in single smooth muscle cells freshly isolated from the stomach of the toad Bufo marinus. When [Ca2+]0 was elevated (> 8mM), action potentials were readily elicited, which had similar characteristics to those found in many tissue preparations of visceral smooth muscle. There was a decrease in membrane resistance at the peak of the action potential and during the undershoot. The following evidence indicated that the inward current is carried by Ca2+: 1) Raising [Ca2+]0 from 15 to 49.6 mM in the presence of 18.2 mM tetraethylammonium chloride (TEA) increased the maximum rate of rise and the overshoot amplitude, the latter by 15 mV, i.e., 29.5 mV/10-fold change in [Ca2+]0. Changing [Na2+]0 from 11.8 to 81.8 mM had no significant effect on the maximum rate of rise or the overshoot. 2) The action potentials were blocked by 8 mM Mn2+ ([Ca2+]0 = 14.6 mM) but not by 14.3 microM tetrodotoxin (TTX) ([Na2+]0 = 100 mM). 3) Action potentials could be elicited when [Ba2+]0 or [Sr2+]0 were present in high concentrations ([Ca2+]0 less than or equal to 31 microM,[Na2+]0 = 11.8 mM). Both the maximum rate of rise and overshoot amplitude of the action potential increased as the membrane potential became more negative, suggesting increased activation of the inward current. Both TEA and Ba2+ prolonged the action potential, suggesting that a K+ current is responsible for repolarization. Action potentials could also be elicited on anode break at elevated [K+]0 (91 mM).

scholarly journals Increase in PNa and PK of Cultured Heart Cells Produced by Veratridine

1969 ◽  
Vol 53 (1) ◽  
pp. 97-114 ◽  
Author(s):  
Nick Sperelakis ◽  
Achilles J. Pappano
Keyword(s):  
Action Potential ◽  
Action Potentials ◽  
Maximum Rate ◽  
Membrane Resistance ◽  
Equilibrium Potential ◽  
Heart Cells ◽  
Anomalous Rectification ◽  
Delayed Rectification ◽  
Cultured Heart Cells ◽  
Maximum Rate Of Rise

Noninnervated cultured chick embryonic heart cells are depolarized by veratridine (10-5 10-6 g/ml) within a few minutes to membrane potentials of -12 ± 2 mv. Action potentials and beating cease. Before depolarization begins, the repolarizing phase of the action potential is prolonged and leads to a long-lasting depolarizing afterpotential, probably due to a holding open of Na+ channels. There is no direct effect on automaticity. Maximum rate of rise of the action potential decreases as a function of the depolarization. The inexcitability is transiently reversed by repolarizing current pulses and by 5 mM Ba++ (but not Sr++) which increases membrane resistance (Rm) and produces a small transient repolarization. Cocaine does not reverse the depolarization. The depolarization also occurs in Cl--free Ringer and in Na+-free Li+-Ringer, but not in Na+-free sucrose-Ringer. In most cases, Rm, measured in the presence and absence of Cl-, initially decreases but sometimes increases. Some of the decrease or increase in gK may be indirectly produced by anomalous or delayed rectification, respectively. Tetrodotoxin, although having no effect on the action potential magnitude or rate of rise, prevents the depolarizing action of veratridine but not its effect on decreasing Rm. It is concluded that veratridine depolarizes by increasing the resting Na+ permeability (PNa); it also tends to increase PK, but this action may be obscured by anomalous rectification when Em is allowed to change. The equilibrium potential for veratridine action is about halfway between ENa and EK, similar to that of acetylcholine at the vertebrate neuromuscular junction.

Acetylcholine lengthens action potentials of sheep cardiac Purkinje fibers

1980 ◽  
Vol 238 (2) ◽  
pp. H237-H243
Author(s):  
S. L. Lipsius ◽  
W. R. Gibbons
Keyword(s):  
Muscarinic Receptors ◽  
Action Potential Duration ◽  
Action Potentials ◽  
Purkinje Fibers ◽  
Diastolic Depolarization ◽  
Cardiac Purkinje Fibers ◽  
Rate Of Increase ◽  
Definite Sequence ◽  
Microelectrode Techniques ◽  
Diastolic Potential

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.

Effects of ischemic conditions and reperfusion on depolarization-induced automaticity

1988 ◽  
Vol 255 (5) ◽  
pp. H992-H999 ◽  
Author(s):  
R. Mohabir ◽  
G. R. Ferrier
Keyword(s):  
Membrane Potential ◽  
Action Potential ◽  
Action Potentials ◽  
Cycle Length ◽  
Slow Inward Current ◽  
Potential Range ◽  
Ischemia And Reperfusion ◽  
Slow Response ◽  
Inward Current ◽  
High Membrane Potential

The inducibility of slow-response automaticity was assessed during ischemic conditions and reperfusion by application of extracellular current. Isolated canine Purkinje fibers were depolarized to membrane potentials less than -65 mV to elicit depolarization-induced automaticity (DIA). Ischemic conditions increased the cycle length of DIA and, in some tissues, prevented sustained DIA or completely abolished DIA. The magnitude of depolarization required to elicit DIA also increased. Inhibition of DIA occurred at a time when action potential plateaus were abbreviated. The effect of reperfusion on DIA was biphasic. Initial reappearance of DIA was followed by inhibition and reduction of the membrane potential range over which DIA could be elicited. Plateaus of action potentials initiated at high membrane potential were abbreviated at this time. DIA returned again as reperfusion effects dissipated. Phasic changes in the inducibility of DIA may represent changes in availability of the slow inward current and may regulate the timing and types of arrhythmic activity occurring with ischemia and reperfusion.

Effects of moderate hypoxia on premature action potentials of rabbit papillary muscle

1984 ◽  
Vol 62 (5) ◽  
pp. 596-599
Author(s):  
Julio Alvarez ◽  
Francisco Dorticós ◽  
Jesús Morlans
Keyword(s):  
Action Potential ◽  
Action Potential Duration ◽  
Action Potentials ◽  
Potassium Current ◽  
Maximum Rate ◽  
Resting Potential ◽  
Papillary Muscles ◽  
Premature Response ◽  
Coupling Interval ◽  
Control Response

Experiments were performed to study the effects of hypoxia on the characteristics of premature action potentials of rabbit papillary muscles. At normal resting potential, the duration of the premature action potential at the shortest coupling intervals was always greater than that of the control response. As the coupling interval was increased beyond 150 ms, the duration of the premature action potential regained control values. In cells depolarized to −70 mV by KCl, early lengthening of the premature response was attenuated. After 60 min of hypoxia, recovery of action potential duration at normal and reduced resting potentials was accelerated. The maximum rate of depolarization and its reactivation time constant were not affected by 60 min of hypoxia. It is suggested that intracellular free Ca is important in the control of action potential duration via the outward background potassium current.

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