Possible role of Na+–Ca2+ exchange in the regulation of contractility in isolated adult ventricular myocytes from rat and guinea pig

1989 ◽  
Vol 67 (12) ◽  
pp. 1525-1533 ◽  
Author(s):  
M. Horackova
Keyword(s):  
Guinea Pig ◽  
Action Potentials ◽  
Ventricular Myocytes ◽  
Contractile Activity ◽  
Strong Dependence ◽  
Tonic Component ◽  
Adult Rat ◽  
Phasic Component ◽  
Single Ventricular Myocytes ◽  
Rat Myocytes

Action potentials and developed contractions of externally unloaded single ventricular myocytes isolated from adult rat and guinea pig hearts were recorded by means of an optical system for recording contractile activity during regular stimulation by microelectrodes. Under control conditions, the shortenings (twitches) in the rat myocytes were fully inhibited by 0.1 μM ryanodine, but they were rather insensitive to the Ca2+ blocker 0.2–0.5 μM nifedipine. In contrast, the contractions of the isolated guinea pig ventricular myocytes were greatly suppressed by 0.2–0.5 μM nifedipine (to <30%), while they were only slightly reduced by 1 μM ryanodine. When the Na+ gradient was decreased by reducing [Na]o or by elevating [Na]i in the presence of veratridine, the twitch contractions were increased in both species. The effect of reduced [Na]o on twitch contractions was not affected by ryanodine in either type of myocytes, while nifedipine still fully abolished the twitches in the guinea pig cells, indicating a strong dependence of guinea pig contractions on Ca2+ influx. On the other hand, the effect of a reduced Na gradient by veratridine was more complex; the usual twitch (phasic component) was increased and it was followed by a second (tonic) component which relaxed only after the repolarization of the action potential. While the phasic component was decreased by nifedipine and ryanodine in the usual way (as in the controls), the sustained contractions (lasting up to several seconds) were ryanodine and nifedipine insensitive. Furthermore, the cardiomyocytes of both species exposed to strontium in place of external calcium still exhibited all the effects observed when reducing the Na+ gradient. These data indicated that Sr2+ transport may occur via various routes similar to those of Ca2+ transport, including the Na+–Sr2+ exchange. In addition, in the presence of SrCl2 the rat myocytes exhibited longer durations of action potentials and their contractions became insensitive to ryanodine (like the guinea pig cells). It is concluded that Na+–Ca2+ exchange probably does not directly contribute in a quantitative fashion to the activation of contractile activity under normal conditions, but when the Na+ gradient is decreased, especially by increasing [Na]i, the contractions could be increased severalfold via this mechanism in both the rat and guinea pig cardiomyocytes.Key words: excitation–contraction coupling, isolated cardiac myocytes, nifedipine, ryanodine, veratridine, reduced [Na]o, epinephrine, SrCl2.

Electrical, contractile, and ultrastructural properties of adult rat and guinea-pig ventricular myocytes in long-term primary cultures

1989 ◽  
Vol 67 (7) ◽  
pp. 740-750 ◽  
Author(s):  
M. Horackova ◽  
C. Mapplebeck
Keyword(s):  
Guinea Pig ◽  
Cultured Cells ◽  
Ventricular Myocytes ◽  
Contractile Activity ◽  
Primary Cultures ◽  
Morphological Characteristics ◽  
Ultrastructural Organization ◽  
Adult Rat ◽  
Intercellular Contacts

The electrical, contractile, and morphological characteristics of ventricular myocytes isolated from adult rat and guinea-pig hearts and maintained in cultures for 7–24 days are described. These cultured cells form different networks, depending on the species, when plated at certain density and maintained under specific conditions; the cells within the networks appear to be electrically coupled. Their resting and action potentials, their contractile activity (shortenings), and their pharmacological responses qualitatively resemble those of freshly isolated myocytes. Cultured cells from both species exhibit near-normal ultrastructural organization of sarcomeres, myofilaments, and mitochondria, as well as formation of intercellular contacts, or gap junctions. These data indicate that cultured adult rat and guinea-pig myocardial cells that make intercellular contacts possess electrical, contractile, and ultrastructural properties and responses to pharmacological agents similar to those of the respective adult myocardial tissues and the functionally intact freshly isolated cells from which these cultures are prepared. Thus, this study indicates that long-term cultures (7–24 days) of networked cardiac myocytes could be used as a valuable experimental model in various investigations of excitation–contraction coupling in cardiac muscle.Key words: cultured adult cardiomyocytes, contractility, electrical activity, ultrastructure, long-term primary cultures.

Effects of estrogen on action potential and membrane currents in guinea pig ventricular myocytes

1999 ◽  
Vol 277 (2) ◽  
pp. H826-H833 ◽  
Author(s):  
Seiko Tanabe ◽  
Toshio Hata ◽  
Masayasu Hiraoka
Keyword(s):  
Guinea Pig ◽  
Action Potential ◽  
Action Potentials ◽  
Voltage Dependence ◽  
Ventricular Myocytes ◽  
Membrane Currents ◽  
Patch Clamp Technique ◽  
17Β Estradiol ◽  
Electrophysiological Effects ◽  
Ionic Basis

To explore a possible ionic basis for the prolonged Q-T interval in women compared with that in men, we investigated the electrophysiological effects of estrogen in isolated guinea pig ventricular myocytes. Action potentials and membrane currents were recorded using the whole cell configuration of the patch-clamp technique. Application of 17β-estradiol (10–30 μM) significantly prolonged the action potential duration (APD) at 20% (APD20) and 90% repolarization (APD90) at stimulation rates of 0.1–2.0 Hz. In the presence of 30 μM 17β-estradiol, APD20 and APD90 at 0.1 Hz were prolonged by 46.2 ± 17.1 and 63.4 ± 11.7% of the control ( n = 5), respectively. In the presence of 30 μM 17β-estradiol the peak inward Ca2+ current ( I CaL) was decreased to 80.1 ± 2.5% of the control ( n = 4) without a shift in its voltage dependence. Application of 30 μM 17β-estradiol decreased the rapidly activating component of the delayed outward K+ current ( I Kr) to 63.4 ± 8% and the slowly activating component ( I Ks) to 65.8 ± 8.7% with respect to the control; the inward rectifier K+ current was barely affected. The results suggest that 17β-estradiol prolonged APD mainly by inhibiting the I Kcomponents I Krand I Ks.

Force measurements from voltage-clamped guinea pig ventricular myocytes

1990 ◽  
Vol 258 (2) ◽  
pp. H452-H459 ◽  
Author(s):  
N. Shepherd ◽  
M. Vornanen ◽  
G. Isenberg
Keyword(s):  
Guinea Pig ◽  
Time Course ◽  
Ventricular Myocytes ◽  
Isometric Force ◽  
Contractile Force ◽  
Patch Clamp Technique ◽  
Thin Glass ◽  
Tonic Component ◽  
Time To Peak ◽  
Whole Cell Patch Clamp

We describe the first observations of isolated mammalian guinea pig ventricular myocytes that combine measurements of contractile force with the voltage-clamp method. The myocytes were attached by poly-L-lysine to the beveled ends of a pair of thin glass rods having a compliance of 0.76 m/N. The contractile force of a cell caused a 1- to 3-microm displacement of the rods; the motion of which was converted to an output voltage by phototransistors. By the use of the whole cell patch-clamp technique, the cells were depolarized at 1 Hz with 200-ms-long clamp pulses from -45 to +5 mV (35 degrees C, 3.6 mM CaCl2). Isometric force began after a latency of 7 +/- 2 ms, peaked at 93 +/- 21 ms, and relaxed (90%) at 235 +/- 63 ms. The time course of force was always faster than that of isotonic shortening (time to peak 154 +/- 18 ms). With 400-ms-long depolarizations, a tonic component was recorded as either sustained force or sustained shortening that decayed on repolarization. Substitution of Ca by Sr in the bath increased the inward current through Ca channels but slowed down the time course of force development. The results are consistent with the hypothesis that activator calcium derives mainly from internal stores and that Ca release needs Ca entry through channels.

Net calcium exchange in adult rat ventricular myocytes: an assessment of mitochondrial calcium accumulating capacity

1984 ◽  
Vol 223 (1231) ◽  
pp. 223-238 ◽  
Keyword(s):  
Calcium Uptake ◽  
Ventricular Myocytes ◽  
Specific Activity ◽  
Strong Dependence ◽  
Mitochondrial Calcium ◽  
Cardiac Mitochondria ◽  
Mitochondrial Membranes ◽  
Adult Rat ◽  
Sudden Rise ◽  
Calcium Exchange

Net calcium exchange has been measured in a suspension of cardiac myocytes after treatment with digitonin. The exchange is believed to be across the mitochondrial membranes and can be stimulated or inhibited by agents augmenting or blocking mitochondrial electron transport. The uptake of calcium shows a strong dependence on suspension p Ca but is not evident below 1 μm ( p Ca 6.0). It is suggested that the net calcium exchange is a balance of the two processes which are equivalent at p Ca 6.0. The measurement of mitochondrial specific activity for calcium uptake allows a calculation of the rapidity with which the cardiac mitochondria would affect sarcoplasmic calcium after a sudden rise. It is suggested that the organelle could partly affect relaxation especially at the peak of contraction.

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