Correction for Silva and Rudy, Circ Res 92 (3) 261-263.

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(Circulation Research. 2003;93:e48.)
© 2003 American Heart Association, Inc.

Correction

In an article by Silva and Rudy (Circ Res. 2003;92:261–263), "Mechanism of Pacemaking in I_K1-Downregulated Myocytes," simulations of ß-adrenergic effects on genetically engineered biological pacemaker cells did not take into account changes in [Ca²⁺]_i due to I_Ca,L increase under ß-adrenergic stimulation (ßAS). Such changes were fully accounted for during pacemaking in the absence of ßAS (intrinsic pacemaker rate of 101 bpm). When ßAS-induced changes in [Ca²⁺]_i were accounted for, a steady state could not be achieved with a 300% I_Ca,L increase. We repeated the simulations with a ßAS-induced 100% increase of I_Ca,L, taking into account the dynamic [Ca²⁺]_i changes. The pacemaking rate increased transiently (110 bpm after 27.2 seconds) and then reached a steady state at a rate slightly below control (73 bpm). The long-term decrease in rate was a result of [Na⁺]_i accumulation that acted to increase outward I_NaK and reduce inward I_NaCa and I_Na, thus reducing net depolarizing current. As in the original publication, upregulation of I_NaCa by 100% increased sensitivity to ßAS, resulting in a maximum transient increase of pacemaking rate to 139 bpm after 17.9 seconds. The new simulations that account for [Ca²⁺]_i changes confirm the original finding that responsiveness to ßAS depends on the level of I_NaCa expression and that even for high expression levels the responsiveness is very limited, much smaller than that of native sinus-node cells

For reference, all simulations used the current version of the Luo-Rudy cell model, which can be found online at http://www.cwru.edu/med/CBRTC/LRdOnline./ [Na⁺]_o was set to 132 mmol/L and [K⁺]_o to 5.4 mmol/L.

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