1. Archive
2. Vol.55, No.6

The Underlying Cellular Mechanism in the Effect of Tetramethylpyrazine on the Anion Secretion of Colonic Mucosa

Abstract: The present study investigated the underlying cellular mechanism in the effect of ligustrazine (tetramethylpyrazine, TMP) on the anion secretion of colonic mucosa in rats using a short-circuit current (I_sc) technique in conjunction with “tool drugs.” (i) After a pretreatment of the tissues by bathing the bilateral surface with Cl⁻-free Krebs-Henseleit (K-H) solution for over an hour, a basolateral application of 1 mmol/l TMP produced an increase in I_sc, and the total charges transported for 30 min were about 8.7 ± 1.4 mC/cm²; an apical pretreatment of DPC and a basolateral addition of acetazolamide decreased the TMP-induced I_sc by about 60% (P < 0.01) and 45% (P < 0.05), respectively; a basolateral application of 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid (DIDS), the inhibitor of Na⁺-HCO₃⁻ cotransporter (NBC), did not alter the TMP-induced I_sc. (ii) After the bilateral surface of mucosa was bathed with HCO₃⁻-free K-H solution for over an hour, a basolateral application of 1 mmol/l TMP produced an increase in I^sc, and the total charges transported in 30 min were about 8.3 ± 1.9 mC/cm²; an apical pretreatment of DPC (1 mmol/l), the inhibitor of Cl⁻ channels, decreased the TMP-induced Isc by about 84% (P < 0.01). The basolateral presence of bumetanide (0.1 mmol/l), the inhibitor of Na⁺-K⁺-Cl⁻ cotransporter (NKCC), significantly reduced the TMP-evoked I_sc by about 86% (P < 0.01). In conclusion, (i) ligustrazine could promote colonic mucosa secretion Cl⁻ via apical Cl⁻ channels and basolateral NKCC; (ii) ligustrazine could promote colonic mucosa secretion HCO₃⁻ via apical Cl⁻ channels and the basolateral diffusion of CO₂.

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