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. 2013 Jan 19;98(2):286–296. doi: 10.1093/cvr/cvt012

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©The Author 2013. Published by Oxford University Press on behalf of the European Society of Cardiology.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by-nc/3.0/), which permits non-commercial use, distribution, and reproduction in any medium, provided that the original authorship is properly and fully attributed; the Journal, Learned Society and Oxford University Press are attributed as the original place of publication with correct citation details given; if an article is subsequently reproduced or disseminated not in its entirety but only in part or as a derivative work this must be clearly indicated. For commercial re-use, please contact journals.permissions@oup.com

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Role of CaMKII and NCX in wave reduction by flecainide. (A) Despite incubation of cells with 1 μM CaMKII inhibitor KN-93, flecainide was still able to significantly reduce Ca²⁺ wave frequency. Magnitude of reduction was similar in the presence of inactive analogue KN-92 (see Supplementary material online, Figure S5A), suggesting CaMKII inhibition is not the mechanism of wave reduction with flecainide. (B) NCX function in terms of Ca²⁺ efflux efficacy was significantly improved following a 5 Hz contraction train in the presence of flecainide. (C) Direct partial inhibition of NCX by 1 mM Ni²⁺ applied after the contraction train increased Ca²⁺ wave frequency. (D) Reduction of [Na⁺]_o after the contraction train can reverse the reduction in wave frequency seen with flecainide. (E) Pooled data from experimental protocol shown in (D) revealing that a reduction in wave frequency induced by flecainide can be reversed by reducing [Na⁺]_o to 125 mM. (F) 0.5 μM veratridine can increase Ca²⁺ wave frequency via enhancing I_Na. This effect was abolished by increasing [Na⁺]_o from 115 to 140 mM.