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.

Embryonic Heart Rate during Development of Domesticated Birds

1991 ◽  
Vol 64 (4) ◽  
pp. 1002-1022 ◽  
Author(s):  
H. Tazawa ◽  
T. Hiraguchi ◽  
O. Kuroda ◽  
S. G. Tullett ◽  
D. C. Deeming
Keyword(s):  
Heart Rate ◽  
Embryonic Heart

Allometric relationships between embryonic heart rate and fresh egg mass in birds

2001 ◽  
Vol 204 (1) ◽  
pp. 165-174 ◽  
Author(s):  
H. Tazawa ◽  
J.T. Pearson ◽  
T. Komoro ◽  
A. Ar
Keyword(s):  
Heart Rate ◽  
Embryonic Heart ◽  
Egg Mass ◽  
Published Data ◽  
Tyto Alba ◽  
Allometric Relationships ◽  
Allometric Relationship ◽  
Subsequent Increase ◽  
Developmental Patterns ◽  
Precocial Birds

Previously, we have measured daily changes (developmental patterns) in embryonic heart rate (fh) in altricial and semi-altricial (ASA) birds (range of mean fresh egg mass approximately 1–20 g), semi-precocial seabirds (egg mass approximately 38–288 g) and precocial birds (egg mass approximately 6–1400 g). An allometric relationship between embryonic fh at 80 % of incubation duration (ID) and fresh egg mass (M) has been derived for six species of precocial bird (fh at 80 % ID=429M(−0.118)). In the present study, additional measurements of embryonic fh in three ASA species, the barn owl Tyto alba, the cattle egret Bubulcus ibis and the lanner falcon Falco biarmicus, were made to extend the egg mass range (20–41 g), and the allometric relationships of embryonic fh for these ASA birds and the precocial and semi-precocial (PSP) groups were investigated from published data. The developmental patterns of embryonic fh in three relatively large ASA species did not show a significant increase prior to the pipping period, unlike those in small ASA birds, but tended to be constant, with a subsequent increase during pipping. The allometric relationship derived for ASA birds was fh at 80 % ID=371M(−0.121) (r=−0.846, P<0.001, N=20) and that for PSP birds was fh at 80 % ID=433M(−0.121) (r=−0.963, P<0.001, N=13). The slopes were parallel, but fh of ASA embryos was low compared with that of PSP embryos with the same egg mass. In ASA birds, embyronic fh was maximal during the pipping (perinatal) period, and the maximum fh (fh(max)) was significantly related to fresh egg mass: fh(max)=440M(−0.127) (r=−0.840, P<0.001, N=20). The allometric relationships for fh at 80 % ID in PSP and fh(max) in ASA embryos were statistically identical. Accordingly, embryonic fh at 80 % ID in PSP birds and fh(max) during pipping in ASA birds can be expressed by a single allometric equation: fh=437M(−0.123) (r=−0.948, P<0.001, N=33).

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.

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.

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