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.

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).

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.

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.

Membrane resistance increases when automaticity develops in explanted rat heart cells

1990 ◽  
Vol 258 (1) ◽  
pp. H145-H152 ◽  
Author(s):  
O. F. Schanne ◽  
M. Lefloch ◽  
B. Fermini ◽  
E. Ruiz-Petrich
Keyword(s):  
Spontaneous Activity ◽  
Action Potentials ◽  
Ventricular Myocytes ◽  
Input Resistance ◽  
Membrane Resistance ◽  
Resting Potential ◽  
Heart Cells ◽  
Membrane Capacity ◽  
Rat Heart Cells ◽  
Specific Membrane

We compared the passive electrical properties of isolated ventricular myocytes (resting potential -65 mV, fast action potentials, and no spontaneous activity) with those of 2- to 7-day-old cultured ventricle cells from neonatal rats (resting potential -50 mV, slow action potentials, and presence of spontaneous activity). In myocytes the specific membrane capacity was 0.99 microF/cm2, and the specific membrane resistance increased from 2.46 k omega.cm2 at -65 mV to 7.30 k omega.cm2 at -30 mV. In clusters, the current-voltage relationships measured under current-clamp conditions showed anomalous rectification and the input resistance decreased from 1.05 to 0.48 M omega when external K+ concentration was increased from 6 to 100 mM. Using the model of a finite disk we determined the specific membrane resistance (12.9 k omega.cm2), the effective membrane capacity (17.8 microF/cm2), and the lumped resistivity of the disk interior (1,964 omega.cm). We conclude that 1) the voltage dependence of the specific membrane resistance cannot completely explain the membrane resistance increase that accompanies the appearance of spontaneous activity; 2) a decrease of the inwardly rectifying conductance (gk1) is mainly responsible for the increase in the specific membrane resistance and depolarization; and 3) approximately 41% of the inward-rectifying channels are electrically silent when spontaneous activity develops in explanted ventricle cells.

Effects of Octopamine on Calcium Action Potentials in Insect Oocytes

1989 ◽  
Vol 142 (1) ◽  
pp. 115-124
Author(s):  
M. J. O'DONNELL ◽  
B. SINGH
Keyword(s):  
Action Potentials ◽  
Rank Order ◽  
Potassium Conductance ◽  
Membrane Resistance ◽  
Threshold Concentration ◽  
Resting Potential ◽  
Calcium Dependent ◽  
Octopamine Receptors ◽  
Voltage Dependent ◽  
Maximum Rate Of Rise

Our experiments show that octopamine receptors are present on the developing follicles of an insect, Rhodnius prolixus. Application of D,L-octopamine decreased the duration and overshoot of calcium-dependent action potentials (APs), and increased the intrafollicular concentration of cyclic AMP. The threshold concentration of D,L-octopamine for the reduction in electrical excitability was between 1 and 5×10−7moll−1, and maximal effects of a 40–50% reduction in AP overshoot and duration were apparent at 10−4moll−1. At concentrations above 10−5moll−1, a small (<10%) hyperpolarization of the resting potential was also apparent. Effects of D,L-octopamine on oocyte excitability were independent of these small shifts in resting potential. Current injection experiments, in which calcium entry was blocked by cobalt, demonstrated that D,L-octopamine reduced membrane resistance at both hyperpolarizing and depolarizing potentials. Octopamine did not affect the maximum rate of rise of the AP, dV/dtmax, which is an indicator of inward calcium current. It is suggested that octopamine may mediate its effects on excitability through an increase in a voltage-dependent potassium conductance. Application of other phenolamines indicated a rank order of potency of D, Loctopamine > D,L-synephrine > tyramine. The α-adrenergic agonists clonidine, naphazoline and tolazoline were without significant effect at 10−5-10−3moll−1. Reduction of excitability by D,L-octopamine was effectively blocked by phentolamine and metoclopramide. Yohimbine and gramine were less effective as antagonists. Possible functions of octopamine receptors in insect follicles are discussed.

scholarly journals Two Components of the Cardiac Action Potential

1969 ◽  
Vol 54 (5) ◽  
pp. 607-635 ◽  
Author(s):  
Antonio Paes de Carvalho ◽  
Brian Francis Hoffman ◽  
Marilene de Paula Carvalho
Keyword(s):  
Action Potential ◽  
Action Potentials ◽  
Time Course ◽  
Slow Component ◽  
Slow Inward Current ◽  
Equilibrium Potential ◽  
Slow Phase ◽  
Positive Equilibrium ◽  
Cardiac Action

Transmembrane potentials recorded from the rabbit heart in vitro were displayed as voltage against time (V, t display), and dV/dt against voltage (V, V or phase-plane display). Acetylcholine was applied to the recording site by means of a hydraulic system. Results showed that (a) differences in time course of action potential upstroke can be explained in terms of the relative magnitude of fast and slow phases of depolarization; (b) acetylcholine is capable of depressing the slow phase of depolarization as well as the plateau of the action potential; and (c) action potentials from nodal (SA and AV) cells seem to lack the initial fast phase. These results were construed to support a two-component hypothesis for cardiac electrogenesis. The hypothesis states that cardiac action potentials are composed of two distinct and physiologically separable "components" which result from discrete mechanisms. An initial fast component is a sodium spike similar to that of squid nerve. The slow component, which accounts for both a slow depolarization during phase 0 and the plateau, probably is dependent on the properties of a slow inward current having a positive equilibrium potential, coupled to a decrease in the resting potassium conductance. According to the hypothesis, SA and AV nodal action potentials are due entirely or almost entirely to the slow component and can therefore be expected to exhibit unique electrophysiological and pharmacological properties.

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