Action Potentials in Heart Cells

2011 ◽  
pp. 163-182 ◽  
Author(s):  
Lars Kaestner ◽  
Qinghai Tian ◽  
Peter Lipp
Keyword(s):  
Action Potentials ◽  
Heart Cells

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.

Injection of guanosine 5'-cyclic monophosphate into heart cells blocks calcium slow channels

1985 ◽  
Vol 248 (5) ◽  
pp. H745-H749 ◽  
Author(s):  
G. Bkaily ◽  
N. Sperelakis
Keyword(s):  
Cyclic Nucleotides ◽  
Action Potentials ◽  
Heart Cells ◽  
Myocardial Cells ◽  
Cyclic Monophosphate ◽  
Intracellular Injection ◽  
Ventricular Cells ◽  
Camp And Cgmp ◽  
Slow Action Potentials

The role of guanosine 5'-cyclic monophosphate (cGMP) in the regulation of the ionic slow channels in heart muscle is less well known than that of adenosine 3,'5'-cyclic monophosphate (cAMP). The effects of intracellular injection of cAMP and cGMP in cultured chick embryonic heart (ventricular) cells by the liposome method were studied. Injection of cAMP into the cells induced spontaneous slow action potentials that could be blocked by verapamil and nifedipine. Injection of cGMP blocked on-going slow action potentials, and this effect was reversed by increasing cAMP. Thus both cAMP and cGMP are involved in the regulation of the slow calcium channels in myocardial cells, and the two cyclic nucleotides are antagonistic.

Calcium antagonist blockade of slow action potentials in cultured chick heart cells

1983 ◽  
Vol 61 (9) ◽  
pp. 957-966 ◽  
Author(s):  
Tung Li ◽  
Nick Sperelakis
Keyword(s):  
Action Potentials ◽  
Rest Period ◽  
Independent Effect ◽  
Heart Cells ◽  
Maximal Effect ◽  
Response Curves ◽  
Dependent Component ◽  
Chick Heart ◽  
Kinetics Of ◽  
Slow Action Potentials

The effects of four Ca antagonists, bepridil, diltiazem, nifedipine, and verapamil, on slow channels were studied in cultured cell reaggregates prepared from 14-day-old chick embryonic, hearts. The cell membrane was partially depolarized to about −45 mV by using 22 mM KCl to inactivate the fast Na+ channels. Slow action potentials were induced by 10−6 M isoproterenol with electrical stimulation. Cumulative dose – response curves for the effect of the four drugs on the blocking of slow action potentials (using [Formula: see text] as the indicator) were analyzed by Hill plots. The dose values for 50% of maximal effect, at a stimulation frequency of 60/min, were (in order of decreasing potencies) as follows: 5.2 × 10−9 M for nifedipine, 3.1 × 10−7 M for diltiazem, 1.2 × 10−6 M for verapamil, and 5.1 × 10−6 M for bepridil. The effect of all four Ca antagonists showed use (or frequency)-dependency, i.e., the drugs were more effective at higher stimulation rates. This may reflect a blocking action of the drugs on the nonresting states of the channels and (or) a slowing of the recovery kinetics of the channels from the inactivated state back to the resting state. In a separate type of experiment utilizing a 5-min rest period in the presence of the drugs, nifedipine blocked and bepridil exhibited some depression of the first action potential elicited, i.e., use-independent effect, indicating that these drugs may also act on resting channels. Thus, these four Ca antagonists have a prominent use-dependent component in their actions, and one or two may also have a use-independent component.

Physiological changes induced in cardiac myocytes by cytotoxic T lymphocytes

1987 ◽  
Vol 252 (1) ◽  
pp. C10-C16 ◽  
Author(s):  
D. Hassin ◽  
R. Fixler ◽  
Y. Shimoni ◽  
E. Rubinstein ◽  
S. Raz ◽  
...  
Keyword(s):  
T Lymphocytes ◽  
Cytotoxic T Lymphocytes ◽  
Action Potentials ◽  
Neonatal Rat ◽  
Mechanical Relaxation ◽  
Heart Cells ◽  
Physiological Changes ◽  
Normal Medium ◽  
Exchangeable Calcium ◽  
Mean Time

The “lethal hit” induced by viral specific, sensitized, cytotoxic T lymphocytes (CTL) attacking virus-infected heart cells is important in the pathogenesis of viral myocarditis and reflects the key role of CTL in this immune response. The mechanisms involved are incompletely understood. Studies of the physiological changes induced in mengovirus-infected, cultured, neonatal, rat heart cells by CTL that had been previously sensitized by the same virus are presented. The CTL were obtained from spleens of mengovirus-infected, major histocompatibility complex (MHC) matched adult rats. Cell wall motion was measured by an optical method, action potentials with intracellular microelectrodes, and total exchangeable calcium content by 45Ca tracer measurements after loading the myocytes with 45Ca and then exposing them to CTL. After 50 min (mean time) of exposing mengovirus-infected myocytes to the CTL, the mechanical relaxation of the myocyte was slowed, with a subsequent slowing of beating rate and a reduced amplitude of contraction. Impaired relaxation progressed, and prolonged oscillatory contractions lasting up to several seconds appeared, with accompanying oscillations in the prolonged plateau phase of the action potentials. Arrest of the myocyte contractions appeared 98 min (mean time) after exposure to CTL. These changes in action potentials and contractions were reversible either by washout with the normal medium or by the addition of verapamil. The amount of total exchangeable calcium in the cultured myocytes, 1 h after exposure to CTL, was significantly increased. This increase was prevented by pretreatment with verapamil. (ABSTRACT TRUNCATED AT 250 WORDS)

Insensitivity of cultured chick heart cells to autonomic agents and tetrodotoxin

1965 ◽  
Vol 209 (4) ◽  
pp. 693-698 ◽  
Author(s):  
Nick Sperelakis ◽  
D. Lehmkuhl
Keyword(s):  
Action Potentials ◽  
Bridge Circuit ◽  
Single Cells ◽  
Heart Cells ◽  
Culture Dish ◽  
Chemical Agents ◽  
Ventricular Cells ◽  
Pacemaker Potentials ◽  
Chick Heart ◽  
Frequency Of Action Potentials

Trypsin-dispersed cells from heart (ventricles) of 7- to 8-day chick embryos and 6-day posthatched chicks were cultured 2–15 days. The isolated single cells became attached to the bottom of the culture dish and reassembled into various monolayer communities; the cells of one community usually contracted synchronously. By means of a bridge circuit, one microelectrode was used for simultaneously passing current and recording membrane potentials. The following chemical agents were electrophysiologically inactive at or below the concentrations indicated (in g/ml): acetylcholine (1.1 x 10–4), epinephrine (2 x 10–4), norepinephrine (3 x 10–4), and tetrodotoxin (1.3 x 10–5). In contrast, 2–7 mm Ba++ (used as a control) was very effective in partially depolarizing the cells, initiating spontaneity, and increasing the frequency of action potentials. Thus, cultured chick ventricular cells, both pacemaker and nonpacemaker, are insensitive to the autonomic agents. The data also suggest that acetylcholine is not necessarily involved in the electrogenesis of pacemaker potentials. The lack of effect of tetrodotoxin is unexplained.

Insulin-specific receptor-mediated slowing of beat rate in embryonic heart cells

1984 ◽  
Vol 246 (3) ◽  
pp. C347-C350 ◽  
Author(s):  
R. L. DeHaan ◽  
G. Goodrum ◽  
E. Strumlauf ◽  
L. J. Elsas
Keyword(s):  
Heart Rate ◽  
Action Potential Duration ◽  
Action Potentials ◽  
Embryonic Heart ◽  
Maximal Response ◽  
Heart Cells ◽  
Specific Receptor ◽  
High Affinity ◽  
Beat Rate ◽  
Pace Maker

Spheroidal aggregates of embryonic heart cells showed their spontaneous beat rate when exposed to insulin. The concentration that produced a half-maximal response (1.7 nM) corresponded to the dissociation constant of binding to a specific high-affinity insulin receptor. The pace-maker phase of action potentials recorded during insulin perfusion was preceded by a prolonged or flattened after hyperpolarization, and its slope was less steep than controls. The action potential duration was also prolonged. These results indicate that physiological concentrations of insulin can regulate the embryonic heart rate.

scholarly journals Intracellular Ca2+ Oscillations, a Potential Pacemaking Mechanism in Early Embryonic Heart Cells

2007 ◽  
Vol 130 (2) ◽  
pp. 133-144 ◽  
Author(s):  
Philipp Sasse ◽  
Jianbao Zhang ◽  
Lars Cleemann ◽  
Martin Morad ◽  
Juergen Hescheler ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Sarcoplasmic Reticulum ◽  
Ryanodine Receptor ◽  
Action Potentials ◽  
Embryonic Heart ◽  
Heart Cells ◽  
Periodic Oscillations ◽  
Mechanical Signals ◽  
Embryonic Cardiomyocytes

Early (E9.5–E11.5) embryonic heart cells beat spontaneously, even though the adult pacemaking mechanisms are not yet fully established. Here we show that in isolated murine early embryonic cardiomyocytes periodic oscillations of cytosolic Ca2+ occur and that these induce contractions. The Ca2+ oscillations originate from the sarcoplasmic reticulum and are dependent on the IP3 and the ryanodine receptor. The Ca2+ oscillations activate the Na+-Ca2+ exchanger, giving rise to subthreshold depolarizations of the membrane potential and/or action potentials. Although early embryonic heart cells are voltage-independent Ca2+ oscillators, the generation of action potentials provides synchronization of the electrical and mechanical signals. Thus, Ca2+ oscillations pace early embryonic heart cells and the ensuing activation of the Na+-Ca2+ exchanger evokes small membrane depolarizations or action potentials.

Nonspecific proteases: a new approach to the isolation of adult cardiocytes

1982 ◽  
Vol 60 (7) ◽  
pp. 997-1002 ◽  
Author(s):  
J. Omar Bustamante ◽  
Toshifumi Watanabe ◽  
Terence F. McDonald
Keyword(s):  
Guinea Pig ◽  
Action Potentials ◽  
Collagenolytic Activity ◽  
Heart Cells ◽  
New Approach ◽  
Adult Heart ◽  
Enzymatic Agents

The potent collagenolytic activity of nonspecific proteinases suggested their use as enzymatic agents for the dissociation of single adult heart cells. This was assessed in guinea pig hearts perfused for 1 min with solutions containing hyaluronidase (100–10000 U/mL), trypsin (100–10000 U/mL), crude collagenase (100–500 U/mL), or nonspecific protease (0.1–100 U/mL). No rod-shaped cells were observed among the cells isolated with these concentrations of hyaluronidase, trypsin, or crude collagenase. By contrast, 45–80% of the cells released with nonspecific protease (5–10 U/mL) were rod shaped and Ca2+ tolerant. Resting and action potentials recorded from cells dispersed with nonspecific protease were similar to those recorded from cells isolated after prolonged collagenase exposure.

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