Summary
The modern view of the mammalian ventricular action potential is that Na-ions are responsible for depolarization, the plateau is maintained by an inward Ca current and repolarization is due to the inactivation of this inward Ca current against a background outward K current. The electrical activity spreads over the surface and T-tubules of the cell and the inflow of Ca-ions, and possibly also the electrical signal, cause, a further release of Ca from internal stores, the lateral cisternae of the sarcoplasmic reticulum (SR). This released Ca, by triggering the splitting of ATP, induces contraction. The released Ca is pumped back into the longitudinal SR and, as the Ca concentration is reduced, relaxation occurs. The Ca in the longitudinal SR is transported back to the storage site in the cisternae. This completes the cycle, release, uptake, transport back to the releasing site. On the basis of this scheme, the action of various drugs is briefly discussed.
The object of any study of the normal electrical processes and of excitation-contraction (EC) coupling is to provide not only a better understanding of normal function but also to give an explanation of pathological disturbances and drug action. While atrium, ventricle and the conducting system of heart all show structural and functional differences, most work on mammalian tissue has been carried out on ventricular muscle andPurkinje fibres. This short review will be confined to mammalian ventricular muscle with only indirect reference to other cardiac tissues. The article will consider the morphology of ventricular cells, then go on to a description of electrical activity and EC coupling. Finally, a brief description of the actions of some drugs on EC coupling will be given. Wherever possible reference will be given to reviews, rather than to individual publications.
Zusammenfassung
Die heutige Ansicht über die Entstehung des AP im Säugermyokard ist wie folgt zu umschreiben: Der Einstrom von Na+ ist für die Depolarisation verantwortlich. Das Plateau wird durch den Ca++-Einstrom unterhalten, und die Repolarisation kommt durch Inaktivierung des Ca++-Einstroms gegenüber einem in dieser Phase konstanten K+-Ausstrom zustande (“background K+ outward current”).
Die Ausbreitung des AP erfolgt mit Sicherheit auf der ganzen Zelloberfläche und (wahrscheinlich) auch in das T-System hinein. Dabei dient der Ca++-Einstrom und eventuell auch das elektrische Signal selber als Triggermechanismus für die Freisetzung gespeicherten Calciums aus zellinternen Speichern (z. B. die lateralen Zysternen des SR). Damit steigt die freie intrazelluläre Ca++-Konzentration, welche ihrerseits die ATP-Spaltung induziert und damit die Kontraktion ermöglicht. Das freigesetzte Ca++ wird in den longitudinalen Anteil des SR zurückgepumpt, so daß die genannte freie [Ca++] wieder vermindert wird und die Erschlaffung stattfinden kann. Das Ca++ wird anschließend von dort in die lateralen Zysternen zurücktransportiert. Damit ist der Kreislauf des intrazellulären Ca++ geschlossen. Auf der Grundlage dieses Modells wird versucht, die Wirkungsweise verschiedener herzwirksamer Stoffe zu erläutern.
This is a preview of subscription content, log in via an institution to check access.
References
Bassingthwaighte, J. B. andH. Reuter, Calcium movements and excitationcontraction coupling in cardiac cells. In: Electrical Phenomena in the Heart, pp. 353–395 (New York-London 1972).
Berger, W., Correlation between the ultrastructure and function of intercellular contacts. In: Electrical Phenomena in the Heart, pp. 63–88 (New York-London 1972).
Blaustein, M. P., Rev. Physiol. Biochem. Pharmacol.70, 33–82 (1974).
Carafoli, E., J. Mol. Cell Cardiol.7, 84–89 (1972).
Fabiato, A. andFrançoise Fabiato, Circulation Res.31, 293–307 (1972).
Fabiato, A. andFrançoise Fabiato, Europ. J. Cardiol.1/2, 143–155 (1973).
Fry, C. H., J. A. S. McGuigan andJ. B. Bassingthwaighte, Control of cardiac action potential by [Ca]i? Union of Swiss Societies for Experimental Biology. Abstracts of the 7th Annual Meeting. Experientia, in press, 1975.
Gergely, J., Circulation Res. 0Suppl.III, 74–82 (1974).
Glitsch, H. G., Pflügers Arch. ges. Physiol.344, 169–180 (1973).
Huxley, A. F., J. Physiol.223, 1–43 (1974).
Isenberg, G. andW. Trautwein, Pflügers Arch. ges. Physiol.350, 41–54 (1974).
Kaufmann, R., R. Bayer, T. Fürniss, H. Krause andH. Tritthart, J. Moll. Cell. Cardiol.6, 543–559 (1974).
Kerrich, W. G. L. andP. M. Best, Scien.183, 435–437 (1974).
Langer, G. A., Girculation46, 180–187 (1972).
Langer, G. A., Amer. Rev. Physiol.35, 55–86 (1973).
Lee, K. S. andW. Klaus, Pharmac. Rev.23, 193–261 (1971).
Legato, M. J. andG. A. Langer, J. Cell. Biol.41, 401–423 (1969).
Lehninger, A. L., Circulat. Res. Suppl. III, 83–90 (1974).
McGuigan, John A. S., J. Physiol.240, 775–806 (1974).
Morad, M. andY. Goldman, Prog. Biophys. molec. Biol.27, 257–313 (1973).
New, W. andW. Trautwein, Pflügers Arch. ges. Physiol.334, 1–23 (1972).
Noble, D. andR. W. Tsien, J. Physiol.200, 233–254 (1969).
Noma, A. andH. Irisawa, Pflügers Arch. ges. Physiol.351, 177–182 (1974).
Page, E. andH. A. Fozzard, The structure and function of muscle. Volume II, ed.Bourne, G. H., pp. 91–158 (New York and London 1973).
Reuter, H., Prog. Biophys. molec. Biol.26, 1–43 (1973).
Reuter, H., Circulat. Res.34, 599–605 (1974a).
Reuter, H., J. Physiol.242, 429–451 (1974b).
Simson, F. O., D. G. Rayns andM. Janet Ledingham, Ultrastructure of the mammalian heart, ed.Challice, C. E. andS. virágh, pp. 1–41 (New York and London 1973).
Trautwein, W., Physiol. Rev.53, 793–835 (1973).
Weidmann, S., Electrical coupling between myocardial cells. In: Prog. Brain Res.31, ed.Akert, K. andP. G. Waser, pp. 275–281 (Amsterdam 1969).
Weidmann, S., Heart: Electrophysiology. Ann. Rev. Physiol.36, 155–169 (1974).
Winegrad, S., J. Gen. Physiol.51, 65–83 (1968).
Winegrad, S., J. Gen. Physiol.55, 77–88, (1970).
Winegrad, S., J. Gen. Physiol.58, 71–93 (1971).
Author information
Authors and Affiliations
Additional information
With 4 figures
Rights and permissions
About this article
Cite this article
Bass, O., McGuigan, J.A.S. Electrical activity and excitation-contraction coupling in mammalian ventricular muscle. Basic Res Cardiol 70, 585–595 (1975). https://doi.org/10.1007/BF01906469
Received:
Issue Date:
DOI: https://doi.org/10.1007/BF01906469