The rapid application of caffeine to cardiac myocytes is commonly used to assess changes in the Ca2+ content of the sarcoplasmic reticulum (SR) and to study other parameters of intracellular Ca2+ regulation. Here we examined the effects of rapid caffeine application on membrane potential, intracellular Ca2+, and cell shortening in ventricular myocytes (rat, rabbit, guinea pig, dog) and atrial myocytes (rabbit) that were not voltage clamped. Conditioning pacing was used to achieve a steady-state level of SR Ca2+ loading prior to caffeine (10 mM) application. Caffeine transiently depolarized myocytes as expected from activation of forward Na+-Ca2+ exchange. However, we also found in each species (50% rat, 36% rabbit ventricular, 53% rabbit atrial, 56% guinea pig, 31% dog) that the caffeine-induced depolarization could also trigger an action potential. Caffeine-triggered potentials were completely blocked by thapsigargin (1 mu M). The Ca2+ transient and contraction that accompanied caffeine-triggered action potentials had a larger magnitude and slower rate of decline (or relaxation) than occurred during caffeine-induced subthreshold depolarizations. Thus, the use of rapid caffeine application to study SR function and [Ca2+](i) regulation in myocytes that are not voltage clamped can yield erroneous results.

Complications associated with rapid caffeine application to cardiac myocytes that are not voltage clamped / Zaniboni, Massimiliano; Yao, A; Barry, Wh; Musso, E; Spitzer, Kw. - In: JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY. - ISSN 0022-2828. - 30:11(1998), pp. 2229-2235. [10.1006/jmcc.1998.0782]

Complications associated with rapid caffeine application to cardiac myocytes that are not voltage clamped.

ZANIBONI, Massimiliano;
1998-01-01

Abstract

The rapid application of caffeine to cardiac myocytes is commonly used to assess changes in the Ca2+ content of the sarcoplasmic reticulum (SR) and to study other parameters of intracellular Ca2+ regulation. Here we examined the effects of rapid caffeine application on membrane potential, intracellular Ca2+, and cell shortening in ventricular myocytes (rat, rabbit, guinea pig, dog) and atrial myocytes (rabbit) that were not voltage clamped. Conditioning pacing was used to achieve a steady-state level of SR Ca2+ loading prior to caffeine (10 mM) application. Caffeine transiently depolarized myocytes as expected from activation of forward Na+-Ca2+ exchange. However, we also found in each species (50% rat, 36% rabbit ventricular, 53% rabbit atrial, 56% guinea pig, 31% dog) that the caffeine-induced depolarization could also trigger an action potential. Caffeine-triggered potentials were completely blocked by thapsigargin (1 mu M). The Ca2+ transient and contraction that accompanied caffeine-triggered action potentials had a larger magnitude and slower rate of decline (or relaxation) than occurred during caffeine-induced subthreshold depolarizations. Thus, the use of rapid caffeine application to study SR function and [Ca2+](i) regulation in myocytes that are not voltage clamped can yield erroneous results.
1998
Complications associated with rapid caffeine application to cardiac myocytes that are not voltage clamped / Zaniboni, Massimiliano; Yao, A; Barry, Wh; Musso, E; Spitzer, Kw. - In: JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY. - ISSN 0022-2828. - 30:11(1998), pp. 2229-2235. [10.1006/jmcc.1998.0782]
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11381/1493604
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