JCS -- Choi et al. 116 (13): 2665 Figure IG3

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Fig. 3. KCl-elicited [Ca²⁺]_c rises through voltage-operated calcium channels. After application of 60 mM KCl for 12 seconds ( ${blacktriangleup}$ ), the KCl solution was reapplied under the presence of L-type Ca²⁺ channel (10 µM nifedipine, A), N-type Ca²⁺ channel (1 µM ${omega}$ -conotoxin GVIA, B), and P/Q-type Ca²⁺ channel (1 µM ${omega}$ -agatoxin IVA, C) antagonists, a cocktail of the above three antagonists (D), or 100 µM CdCl₂ (E). (F) Summary of the inhibitions of the KCl-elicited [Ca²⁺]_c rises by VOCC antagonists; nifedipine (36.0±3.0% of control, n=10), ${omega}$ -conotoxin GVIA (69.5±8.8%, n=5), ${omega}$ -agatoxin IVA (92.3±6.6%, n=4), cocktail of the above three antagonists (23.2±4.1%, n=3), and CdCl₂ (15.0±2.7%, n=4). *Significant difference (paired student t-test, P<0.05). Nif, nifedipine; ${omega}$ -cono GVIA, ${omega}$ -conotoxin GVIA; ${omega}$ -aga IVA, ${omega}$ -agatoxin IVA.