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Caffeine induces a transient inward current in cultured cardiac cells

Nature volume 301, pages 248250 (20 January 1983) | Download Citation

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Abstract

Electrical excitation of cardiac muscle may sometimes be due to initiation of inward current by the presence of Ca2+ ions at the inner surface of the cell membrane. During digitalis toxicity and other conditions that abnormally augment cellular Ca2+ stores, premature release of Ca2+ from the sarcoplasmic retkulum leads to a transient inward current, which is large enough to initiate premature beats and is accompanied by a transient contractile response1–5 This inward current may be mediated either by electrogenic sodium–calcium exchange6 or by specific Ca2+-activated cation channels that have recently been characterized in tissue cultures of cardiac myocytes7. An obvious question raised by these observations is whether release of the sequestered Ca2+ stores during each normal beat exerts a similar influence on membrane potential. To explore this, chick embryonic myocardial cell aggregates were voltage-clamped during abrupt exposure to caffeine, which is known to release Ca2+ from the sarcoplasmic reticulum8–10. The speed of the perfusion system and the relative absence of diffusion barriers in the tissue-cultured cells allowed the effects of caffeine-induced Ca2+ release to be studied on a time scale comparable to that of a single normal beat. We report here that abrupt exposure of the cells to caffeine produced a transient inward current having similar features to that of digitalis toxicity, and which was both large enough and rapid enough to potentially contribute to the action potential.

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Affiliations

  1. Division of Cardiology, Stanford University Medical School, Stanford, California 94305, USA

    • William T. Clusin

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About this article

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DOI

https://doi.org/10.1038/301248a0

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