Aim To investigate the vasodilatory effect of Ferulic acid on in vitro rat coronary artery and its possible mechanism. Methods By using the mi-crovessel tension recorder system, the vasodilatory effect of FA on resting and contractin-vitro rat coronary artery was determined;the influence of endothelial in-tegrity to FA-induced vasorelaxation was observed; the relationship of FA on [ Ca2+] ex-influx-induced and [ Ca2+] in-efflux-induced contractions was discussed;the mechanism of vasodilatory effect of FA was ex-plored by applying the inhibitors of KCa(TEA),KATP channel ( Gli ) , KIR channel ( BaCl2 ) , KV ( 4-AP ) , NOS( L-NAME) and COX( Indo) . Results FA had no effect on the resting tension of in vitro rat coronary artery. FA dilated the in-vitro rat coronary artery pre-treated with KCl ( 60 mmol · L-1 ) , U46619 ( 1 μmol · L-1 ) and PE ( 10μmol · L-1 ) in a concentration-dependent fashion ( P < 0. 05 ) . FA inhibited the [ Ca2+] ex-influx-induced and [ Ca2+] in-efflux-in-duced contractions significantly ( P <0. 05 ) . 4-AP ( 1 mmol· L-1 ) restrained the diastolic function of FA, while TEA, Gli, BaCl2、L-NAME, Indo had no obvious effect ( P >0. 05 ) . Conclusion The diastolic func-tion could be related to the activation of KV channel on vascular smooth muscle cells, the free Ca2+ from Sar-coplasmic reticulum cells and blockade extracellular Calcium channel do not depend on KCa, KATP, KIR channel, nor the endothelial function.

AIM:To explore the mechanisms underlying contraction induced by extracelluar acidosis (pHex6.8) in rat isolated coronary artery (RCA).METHODS:Using the microvessel tension recorder system, the effects of acid-base transporters on RCA contraction induced by pHex6.8 were explored by applying the selective pharmacological inhibitors of Na+-H+ exchanger 1 (NHE-1) and Na+-HCO-3 cotransporter (NBC), HOE-642 and S0859, respectively.The effects of chloride channel on RCA contraction induced by pHex6.8 were explored by applying the inhibitors of chloride channel (NPPB and NFA), and by replacing the extracellular NaCl with equimolar NaBr.RESULTS:pHex6.8 augmented the resting tension of RCA, and the maximum contraction was (3.90±0.95) mN.HOE-642 at 30 μmol/L and S0859 at 100 μmol/L both inhibited the contraction of RCA induced by pHex6.8 (P<0.01).NPPB and NFA both inhibited the contraction of RCA induced by pHex6.8 or KCl (60 mmol/L) in a concentration-dependent manner.NPPB and NFA (100 μmol/L) both inhibited the contraction of RCA induced by U46619 (1 μmol/L).Replacing the extracellular NaCl with equimolar NaBr almost completely inhibited RCA contraction induced by pHex6.8 (P<0.01), but had no obvious effect on the contraction induced by KCl (60 mmol/L) or U46619 (1 μmol/L).CONCLUSION:Extracellular acidosis-induced contraction in RCA may be related to the activated NHE-1 and NBC, and it may be also related to the enhanced chloride transport across the membrane.