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. 2008 Oct;132(4):397–405. doi: 10.1085/jgp.200809960

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© 2008 Rapila et al.

This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.jgp.org/misc/terms.shtml). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).

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Figure 5. — Plasmalemmal calcium influx is needed to maintain the SR calcium stores when calcium is extruded by the NCX. (A) L-type calcium channel inhibitor nifedipine (10 μM) suppresses spontaneous calcium signals (bottom left), modulates the shape of APs, and eventually inhibits AP generation. (B) This is accompanied by simultaneous depletion of SR calcium content as estimated by rapid application of caffeine (n = 24 control plus 8 nifedipine). (C) When the NCX is blocked (with Ni²⁺) together with inhibition of L-type calcium channels (with nifedipine; bottom left), embryonic cardiomyocytes retain their spontaneous activity longer compared with the application of nifedipine alone (top left). This is measured as the number of spontaneous oscillations before the calcium-transient amplitude is reduced to 50% of its original value (right).