Inhibitory effect of opioids on sympathetic neurotransmission in the bovine iris
Inhibitory effect of opioids on sympathetic neurotransmission in the bovine iris
复制标题
阿片类药物对牛虹膜交感神经传递的抑制作用
DOI:
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发表时间:
1996
期刊:
影响因子:
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通讯作者:
S. Ohia
中科院分区:
文献类型:
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作者:
F. Anderson;S. Rice;C. Opere;K. al;S. Ohia
We investigated the effect of opioids and related peptides on sympathetic neurotransmission in the isolated, superfused bovine iris. Furthermore, we evaluated the use of the bovine iris as a possible model for pharmacological studies of norepinephrine (NE) release from sympathetic nerves. Electrical stimulation of irides preloaded with [ 3 H]NE caused an increase in tritium efflux over basal levels. Chromatographic analysis of released radioactive material showed that unmetabolized NE accounted for 46.1 ± 9.3% (n=5) of total tritium efflux from superfused tissues. Thus, field stimulation-induced tritium efflux was designated as [ 3 H]NE release. Electrically-evoked [ 3 H]NE overflow was attenuated when the external calcium concentration was lowered below 1.3 mM or in the presence of omega conotoxin (but not nitrendipine) indicating that an influx of calcium via voltage-dependent neuronal channels is necessary for NE release from sympathetic nerves in the bovine iris. All opioid agonists tested suppressed field stimulation-evoked [ 3 H]NE release with the following rank order of potency : bremazocine >[D-Ala 2 , D-Leu 5 ]-enkephalin > [D-Ala 2 , MePhe 4 , Gly-ol 5 ]-enkephalin > morphine. Naloxone (1 μM) abolished the inhibition of NE release caused by submaximal concentrations of bremazocine or morphine. We conclude that opioid agonists impair sympathetic neurotransmission in the bovine iris by interacting with prejunctional opioid receptors.