Tyrosine nitration results in altered function of selective proteins, including human smooth muscle L‐type calcium channel, hCav1.2b. We report here that Cav1.2 is also subject to “denitration”. Cell lysates from activated macrophage‐like cell line, RAW264.7 cells, reversed peroxynitrite‐induced nitration of the carboxy terminus of Cav1.2 in a 1D gel assay. Tyrosine phosphorylation of the calcium channel by c‐src kinase was blocked by nitration but reversed by pretreatment with RAW264.7 cell lysates. These findings indicate that denitration may be a physiological mechanism to restore cellular excitability during inflammation.