Excitation-contraction coupling in voltage-clamped cardiac myocytes

Myocytes isolated from guinea pig ventricles were voltage-clamped using patch pipettes in the whole-cell configuration. For proper voltage control fast Na+ current was blocked by TTX or inactivated by an appropriate prepulse. Zero-load cell shortening was monitored by a photoelectric device. The mec...

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Bibliographic Details
Published in:Basic research in cardiology 1989-03, Vol.84 (2), p.136-148
Main Authors: MEYER, R, HAAS, H. G, WIEMER, J
Format: Article
Language:English
Subjects:
Action Potentials
Animals
Biological and medical sciences
Calcium - metabolism
Electricity
Fundamental and applied biological sciences. Psychology
Guinea Pigs
Heart
Heart - physiology
Myocardial Contraction
Myocardium - cytology
Sarcoplasmic Reticulum - physiology
Space life sciences
Ventricular Function
Vertebrates: cardiovascular system
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Summary:Myocytes isolated from guinea pig ventricles were voltage-clamped using patch pipettes in the whole-cell configuration. For proper voltage control fast Na+ current was blocked by TTX or inactivated by an appropriate prepulse. Zero-load cell shortening was monitored by a photoelectric device. The mechanical response to a short depolarizing clamp was mainly a phasic (transient) contraction. Long-lasting depolarizations caused a tonic (sustained) shortening of a cell. Different clamp patterns were used to study the mode of activation of phasic contraction. 1) With a constant Ca2+ preload established by a train of conditioning pulses, the shortening-voltage relation measured with test pulses of varying height was a bell-shaped curve reflecting the slow inward current (ICa)-voltage relation. The test pulse had a striking influence on the first contraction of the following conditioning series, resulting in an S-shaped relation between post-test contraction and test potential. 2) With series of identical clamps of varying height, steady-state contraction was maximal around 40 mV and not in proportion to ICa. In these measurements Ca2+ preload was likely to increase with increasing potential. It is concluded that ICa initiates phasic contraction by inducing a release of Ca2+ from internal stores while replenishment of the stores is largely determined by an electrogenic transsarcolemmal Na+-Ca2+ exchange. The data suggest that Na+-Ca2+ exchange is not only involved in long-term changes of cardiac contractility but also in beat-to-beat regulation.
ISSN:0300-8428
1435-1803
DOI:10.1007/BF01907923