Nedergaard O A
Department of Pharmacology, School of Medicine, Odense University, Denmark.
Pharmacol Toxicol. 1988 Nov;63(5):317-23. doi: 10.1111/j.1600-0773.1988.tb00961.x.
The aim of this study was to examine the modulating role of presynaptic alpha 2-adrenoceptors on transmitter release from vascular sympathetic neurones. This was done by examining the influence of removal of inactivation pathways on the effect of alpha-adrenoceptor antagonists on the release of transmitter from noradrenergic neurones. The rabbit main pulmonary artery preloaded with 3H-noradrenaline (3H-NA) was used. The artery was stimulated with 300 pulses at various frequencies (1, 3, 10 and 30 Hz). Pargyline (3 x 10(-4) M) increased the stimulation-evoked 3H-overflow at 1 and 3 Hz and decreased it at 30 Hz. U-0521 (3',4'-dihydroxy-2-methylpropiophenone; 3 x 10(-6) M) enhanced the overflow at 1 Hz and had no effect at 3-30 Hz. Corticosterone (4 x 10(-5) M) did not alter the stimulation-evoked 3H-overflow at 1-30 Hz. Cocaine (3 x 10(-6) M) enhanced the 3H-overflow slightly at 1-30 Hz. At 3 x 10(-5) M, cocaine enhanced 3H-overflow at 1 Hz and reduced it at 30 Hz. Neither corticosterone (4 x 10(-5) M) nor propranolol (10(-7) M) modified this effect of cocaine. Propranolol (10(-7) M) alone decreased the 3H-overflow at 30 Hz and had no effect at 1-10 Hz. Phenoxybenzamine (10(-6) M) and chlorpromazine (3 x 10(-6) M) potentiated the stimulation-evoked 3H-overflow at 1-30 Hz.(ABSTRACT TRUNCATED AT 250 WORDS)
本研究的目的是检测突触前α2 -肾上腺素能受体对血管交感神经元递质释放的调节作用。通过研究去除失活途径对α -肾上腺素能受体拮抗剂对去甲肾上腺素能神经元递质释放作用的影响来实现这一目的。使用预先加载3H -去甲肾上腺素（3H - NA）的兔主肺动脉。以不同频率（1、3、10和30 Hz）施加300个脉冲刺激该动脉。帕吉林（3×10(-4) M）在1和3 Hz时增加刺激诱发的3H溢出，在30 Hz时降低。U - 0521（3'，4'-二羟基-2 -甲基苯丙酮；3×10(-6) M）在1 Hz时增强溢出，在3 - 30 Hz时无作用。皮质酮（4×10(-5) M）在1 - 30 Hz时不改变刺激诱发的3H溢出。可卡因（3×10(-6) M）在1 - 30 Hz时轻微增强3H溢出。在3×10(-5) M时，可卡因在1 Hz时增强3H溢出，在30 Hz时降低。皮质酮（4×10(-5) M）和普萘洛尔（10(-7) M）均未改变可卡因的这种作用。单独使用普萘洛尔（10(-7) M）在30 Hz时降低3H溢出，在1 - 10 Hz时无作用。酚苄明（10(-6) M）和氯丙嗪（3×10(-6) M）在1 - 30 Hz时增强刺激诱发的3H溢出。（摘要截选至250字）
