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

An extract of the first 250 words of the full text is provided, because this article has no abstract.

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 . . . [Full Text of this Article]