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(1) Butylidenephthalide (Bdph) concentraction-dependently

Butylidenephthalide 在離體狗血管的鬆弛作用 Relaxant Effects of Butylidenephthalide in Isolated Dog Blood Vessels. (1) Butylidenephthalide (Bdph) concentraction-dependently relaxed the isolated dog saphenous vein (SV), coronary artery (CA), femoral artery (FA) and mesentric artery (MA),

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(1) Butylidenephthalide (Bdph) concentraction-dependently

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  1. Butylidenephthalide 在離體狗血管的鬆弛作用Relaxant Effects of Butylidenephthalide in Isolated Dog Blood Vessels • (1) Butylidenephthalide (Bdph) concentraction-dependently • relaxed the isolated dog saphenous vein (SV), coronary artery • (CA), femoral artery (FA) and mesentric artery (MA), • precontracted by KCl (60 mM) and phenylephrine (phe, 5 μM) with • an exception of CA by prostaglandin F2α (PGF2α, 2 μM) instead • of phe. The potency order of Bdph to these blood vessels was SV> • CA>FA, MA. There was a significant difference among these four • tissues with an exception between FA and MA. • (2) Bdph also non-competitively inhibited cumulative KCl (5-120 • mM)- and phe (0.1-100 μM)-induced contractions in these four • blood vessels excluding CA to phe. Roughly, the potency order of • Bdph to these blood vessels roughly was SV, CA>FA, MA. There was • a significant difference between the former two and the latter • two, though no significant differences found between the former • two and between the latter two. • (3) There was also no significant difference between -logIC50 • and PD2' values in each tissue. It suggests that inhibitory • effects of Bdph on Ca2+-influx through voltage (VOC) and/or • receptor operated calcium channels (ROC) may be similar to those • on Ca2+-release from calcium stores in each tissue. Bdph also • non-competitively inhibited cumulative Ca2+-induced contractions • in depolarized preparations. The potency order was SV>CA>FA, MA.

  2. (4) The relaxing effects of Bdph was endothelium independent. • There was no correlation to opening of ATP- and/or Ca2+- • sensitive potassium channels and to activation of adenylate and/ • or guanylate cyclase. • (5) Bdph dose-dependently and parallelly leftward shifted the • log dose-response curve of forskolin (FK) in SV or CA, and • reduced the IC50 of FK. Bdph parallelly leftward shifted the log • dose-response curves of sodium nitroprusside (SNP) in CA or FA • and reduced the IC50 of SNP. Bdph (200 μM) significantly • enhanced the cAMP content in SV, Bdph (500 μM) significantly • enhanced the cAMP and cGMP contents in CA, and Bdph (1000 μM) • significantly enhanced cGMP content in FA. These results suggest • that relaxant fect of Bdph may be related to inhibiting cAMP- • dependent phosphodiesterase (PDE) activity in SV or CA and to • inhibiting cGMP-dependent PDE activity in CA or FA. • (6) The above results suggest that the higher selectivities of • Bdph to SV and CA than to FA and MA, after Bdph administration • in vivo, the reduction in venoreturn and the increase in • coronary flow may occur without affecting FA and MA. Therefore • Bdph may be useful in the treatment of angina pectoris without • affecting blood pressure. Further studies are needed to • elucidate its action mechanisms. • Key words: Butylidenephthalide, dog blood vessels, Ca2+ influx, • Ca2+ release, cAMP- • dependent phosphodiesterase, cGMP-dependent phosphodiesterase

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