Prejunctional alpha2-adrenoceptors and peroxide-induced potentiation of norepinephrine release from the bovine iris.
Prejunctional alpha2-adrenoceptors and peroxide-induced potentiation of norepinephrine release from the bovine iris.
复制标题
交界前α2-肾上腺素受体和过氧化物诱导的牛虹膜去甲肾上腺素释放增强。
DOI：
10.1023/a:1020764220449
复制
发表时间：
1998
影响因子：
4.4
通讯作者：
Ohia,SE
中科院分区：
文献类型：
--
作者：
Opere,CA;Ohia,SE
过氧化物可以增强来自几种哺乳动物的虹膜中场刺激的 [3H] 去甲肾上腺素 ([3H]NE) 释放。在本研究中，我们研究了连接前α2-肾上腺素受体在牛离体虹膜中过氧化物诱导的交感神经传递增强中的作用。分离的半虹膜在含有 [3H]NE 的 Krebs 缓冲溶液中孵育，并为使用灌注法研究神经递质释放做好准备。 α2-肾上腺素受体激动剂、羟甲唑啉、UK-14304 和可乐定可抑制场刺激的 [3H]NE 溢出，而不影响基础氚流出。用H2O2(300 μM)预处理组织对抑制由α2-肾上腺素能激动剂引起的[3H]NE释放没有影响。然而，H2O2(300 μM) 导致育亨宾 (10 nM–1 μM) 的兴奋浓度-反应曲线显着左移 (P < 0.01)。相比之下，育亨宾（1μM）并不能阻止H2O2（300μM）引起的[3H]NE溢出的增强。总之，过氧化物对牛虹膜交感神经传递的兴奋作用不是由交界前 α2-肾上腺素受体介导的。
Peroxides can enhance field-stimulated [3H]norepinephrine ([3H]NE) release in isolated irides from several mammalian species. In the present study, we investigated the role of prejunctional α2-adrenoceptors in peroxide-induced potentiation of sympathetic neurotransmission in bovine isolated irides. Isolated hemi-irides were incubated in a Krebs buffered-solution containing [3H]NE and prepared for studies of neurotransmitter release using the superfusion method. α2-Adrenoceptor agonists, oxymetazoline, UK-14304 and clonidine inhibited field-stimulated [3H]NE overflow without affecting basal tritium efflux. Pretreatment of tissues with H2O2(300 μM) had no effect on inhibition of evoked [3H]NE release caused by the α2-adrenergic agonists. However, H2O2(300 μM) caused significant (P < 0.01) leftward shifts of excitatory concentration-response curves to yohimbine (10 nM–1 μM). In contrast, yohimbine (1 μM) did not prevent the enhancement of evoked [3H]NE overflow induced by H2O2(300 μM). In conclusion, excitatory effects of peroxides on sympathetic neurotransmission in bovine irides are not mediated by prejunctional α2-adrenoceptors.