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Background  Apamin is commonly used as a small-conductance Ca 2+ -activated K +  (SK) current inhibitor. However, the specificity of apamin in cardiac tissues remains unclear.    Objective  To test the hypothesis that apamin does not inhibit any major cardiac ion currents.    Methods  We studied human embryonic kidney (HEK) 293 cells that expressed human voltage-gated Na + , K +  and Ca 2+  currents and isolated rabbit ventricular myocytes. Whole-cell patch clamp techniques were used to determine ionic current densities before and after apamin administration.    Results  Ca 2+  currents (CACNA1c+CACNB2b) were not affected by apamin (500 nM) (data are presented as median [25 th  percentile;75 th  percentile] (from –16 [–20;–10] to –17 [–19;–13] pA/pF, P = NS), but were reduced by nifedipine to –1.6 [–3.2;–1.3] pA/pF (p = 0.008). Na +  currents (SCN5A) were not affected by apamin (from –261 [–282;–145] to –268 [–379;–132] pA/pF, P = NS), but were reduced by flecainide to –57 [–70;–47] pA/pF (p = 0.018). None of the major K +  currents ( I   Ks ,  I   Kr ,  I   K1  and  I   to ) were inhibited by 500 nM of apamin (KCNQ1+KCNE1, from 28  [20] ;  [37]  to 23  [18] ;  [32]  pA/pF; KCNH2+KCNE2, from 28  [24] ;  [30]  to 27  [24] ;  [29]  pA/pF; KCNJ2, from –46 [–48;–40] to –46 [–51;–35] pA/pF; KCND3, from 608 [505;748] to 606 [454;684]). Apamin did not inhibit the  I   Na  or  I   CaL  in isolated rabbit ventricular myocytes ( I   Na,  from –67 [–75;–59] to –68 [–71;–59] pA/pF;  I   CaL , from –16 [–17;–14] to –14 [–15;–13] pA/pF, P = NS for both).    Conclusions  Apamin does not inhibit human cardiac Na +  currents, L-type Ca 2+  currents or other major K +  currents. These findings indicate that apamin is a specific SK current inhibitor in hearts as well as in other organs.

Apamin Does Not Inhibit Human Cardiac Na+ Current, L-type Ca2+ Current or Other Major K+ Currents