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  • Title: Effects of chloride channel blockers on hypotonicity-induced contractions of the rat trachea.
    Author: Coelho RR, Souza EP, Soares PM, Meireles AV, Santos GC, Scarparo HC, Assreuy AM, Criddle DN.
    Journal: Br J Pharmacol; 2004 Jan; 141(2):367-73. PubMed ID: 14691057.
    Abstract:
    1. We have investigated the inhibitory effects of blockers of volume-activated (Cl(vol)) and calcium-activated (Cl(Ca)) chloride channels on hypotonic solution (HS)-induced contractions of rat trachea, comparing their effects with those of the voltage-dependent calcium channel (VDCC) blocker nifedpine. 2. HS elicited large, stable contractions that were partially dependent on the cellular chloride gradient; a reduction to 41.45+/-7.71% of the control response was obtained when extracellular chloride was removed. In addition, HS-induced responses were reduced to 26.8+/-5.6% of the control by 1 microm nifedipine, and abolished under calcium-free conditions, indicating a substantial requirement for extracellular calcium entry, principally via VDCCs. 3. The established Cl(vol) blockers tamoxifen (</=10 microm) and 4,4'-diisothiocyanatostilbene-2,2'-disulphonic acid (1-100 microm), at concentrations previously reported to inhibit Cl(vol) in smooth muscle, did not significantly inhibit HS-induced contractions. 4. In contrast, the recognized Cl(Ca) blocker niflumic acid (NFA; 1-100 microm) produced a reversible, concentration-dependent inhibition of HS responses, with a reduction to 36.6+/-6.4% of control contractions at the highest concentration. The mixed Cl(vol) and Cl(Ca) blocker, 5-nitro 2-(3-phenylpropylamine) benzoic acid (NPPB; 10-100 microm) also elicited concentration-related inhibition of HS-induced contractions, producing a decrease to 35.9+/-11.3% of the control at 100 microm. 5. Our results show that HS induces reversible, chloride-dependent contractions of rat isolated trachea that were inhibited by NFA and NPPB, while exhibiting little sensitivity to recognized blockers of Cl(vol). The data support the possibility that opening of calcium-activated chloride channels under hypotonic conditions in respiratory smooth muscle may ultimately lead to VDCC-mediated calcium entry and contraction.
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