N-(p-amylcinnamoyl)anthrandic acid (ACA), a phospholipase A(2) (PLA(2)) inhibitor, is structurally-related to non-steroidal anti-inflammatory drugs (NSAIDs) of the fenamate group and may also modulate various ion channels We used the whole-cell, patch-clamp technique at room temperature to investigate the effects of ACA on the Ca2+-activated chloride current (I-CI(Ca)) and other chloride currents in isolated pig cardiac ventricular myocytes ACA reversibly inhibited I-CI(Ca) in a concentration-dependent manner (IC50 = 4 2 mu M, n(Hill) = 1 1), without affecting the L-type Ca2+ current Unlike ACA, the non-selective PLA(2) inhibitor bromophenacyl bromide (BPB, 50 mu M) had no effect on I-CI(Ca) In addition, the analgesic NSAID structurally-related to ACA, diclofenac (50 mu M) also had no effect on I-CI(Ca), whereas the current in the same cells could be suppressed by chloride channel blockers flufenamic acid (FFA, 100 mu M) or 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS, 100 mu M) Besides I-CI(Ca), ACA (50 mu M) also suppressed the cAMP-activated chloride current, but to a lesser extent It is proposed that the inhibitory effects of ACA on I-CI(Ca) are PLA(2)-independent and that the drug may serve as a useful tool in understanding the nature and function of cardiac anion channels (C) 2010 Elsevier Inc All rights reserved