Abstract: AIM: To observe the inhibitory effect of botulinum toxin type A (BTX-A)on rabbit aortic contractility- induced by methoxamine (MOA), an agonist of noradrenergic αreceptor, and electric field stimulation (EFS) in vitro.METHODS: MOA and EFS treated groups were carried out in this study.0.5 cm ×3.0 cm spiral-shaped strip of rabbit abdominal aorta was suspended in incubation bath containing Krebs bicarbonate buffer (pH 7.4, constant 37 ℃)with 95 % O₂ and 5 %CO₂, and the change of muscular force was recorded.Strips in MOA-treated group were administrated with MOA 5 μmol/L for promoting contraction for 30 min, followed by Krebs (as control, n =10), BTX-A 50 U mL (n =10)or 100 U mL (n =10)addition for 30 min recording, and subsequently treated with MOA 5 μmol/L again.Other strips in the EFS treated group were persistently stimulated by 50 Hz, 80 V, 1 ms and 60 s electricity, followed by Krebs (n = 10)or BTX-A 50 U mL (n =10)addition for 30min, and subsequently treated with MOA 5 μmol/L again. RESULTS: BTX-A given at 50 and 100 U mL was dose-dependently decreased aortic contractility-induced by MOA by 80 %(P <0.01)and 95 %(P <0.01), respectively.The contractile tension of the strips-treated with BTX-A at 50 and 100 U mL induced by MOA wer 35 %(P <0.01)and 3 %(P <0.01)respectively in comparison with control group.The aortic contractility- induced by EFS was decreased by 94 %(P < 0.01)with BTX-A 50 U mL.The contractile tension MOA repeated addition into the strips-treated with EFS +BTX-A at 50 U mL were decreased to 10 % (P < 0.01)in comparison with control group.CONCLUSION: MOA, an agonist of noradrenergic αreceptor, and EFS, can promote rabbit aortic contractility.BTXA inhibits arterial smooth muscular contractility-induced by MOA and EFS,which is related to inhibiting noradrenergic release and its receptor.

Key words: botulinum toxin type A, aorta, electrical field stimulation, noradrenaline