摘要
After 20min electric field stimulation,L-enkephalin （L-ENK） content in the rabbitear artery declined from the control value of 38.99±17.29 to 12.55±1.96pg/mg of wet tissue（n=12）,and M-enkephalin （M-ENK） content from 134.67±8.11 to 73.68±17.96pg/mg of wet tis-sue （n=6）,both being significantly decreased.This effect was not influenced after blockade ofadrenergic receptor by yohimbine.Contractions of artery strips induced by electric field stimulationwere enhanced distinctly after pretreatment of the artery strips with naloxone,an opioid receptorblocker,and with pronase,but not after pretreatment with trypsin.The results suggested that the re-lease of endogenous enkephalins in the ear artery could be induced by electric field stimulation andx<sub>2</sub>-receptor might not participate in the release course,The release amount of ENK from the ar-terv strips increased when the stimulus freduency increased within the range of 2 Hz to 8 Hz.
After 20min electric field stimulation,L-enkephalin (L-ENK) content in the rabbit ear artery declined from the control value of 38.99±17.29 to 12.55±1.96pg/mg of wet tissue (n=12),and M-enkephalin (M-ENK) content from 134.67±8.11 to 73.68±17.96pg/mg of wet tis- sue (n=6),both being significantly decreased.This effect was not influenced after blockade of adrenergic receptor by yohimbine.Contractions of artery strips induced by electric field stimulation were enhanced distinctly after pretreatment of the artery strips with naloxone,an opioid receptor blocker,and with pronase,but not after pretreatment with trypsin.The results suggested that the re- lease of endogenous enkephalins in the ear artery could be induced by electric field stimulation and x_2-receptor might not participate in the release course,The release amount of ENK from the ar- terv strips increased when the stimulus freduency increased within the range of 2 Hz to 8 Hz.
