Potentiation of sympathetic neurotransmission in bovine isolated irides by isoprostanes.
Potentiation of sympathetic neurotransmission in bovine isolated irides by isoprostanes.
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异前列烷增强牛离体虹膜交感神经传递。
DOI：
10.1080/10715760100300791
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发表时间：
2001
影响因子：
3.3
通讯作者：
Ohia,SE
中科院分区：
文献类型：
--
作者：
Opere,CA;Awe,SO;Harris,LC;LeDay,AM;Ohia,SE
异前列腺素（IsoP）是由花生四烯酸的自由基催化过氧化反应形成的，不依赖于环氧合酶。在本研究中，我们研究了IsoP对牛离体虹膜释放去甲肾上腺素（NE）的影响。此外，我们研究了IsoP在过氧化氢（H2 O2）诱导的NE从该组织释放的增强中的作用。制备了牛虹膜，用于使用灌流法研究[3 H]NE释放。通过电场刺激诱导[3 H]NE的释放。8-异前列腺素E2（E2-IsoP）和8-异前列腺素F2α（F2-IsoP）均能使离体牛虹膜的场刺激[3 H]NE释放产生浓度相关性增强，血栓烷（Tx）受体激动剂U46619和H2 O2可模拟这种效应。Tx受体拮抗剂SQ 29548抑制E2-IsoP（10μM）的反应，IC 50为370±50 nM。SQ 29548（10μM）还可以阻断U46619（10μM）诱导的电诱发[3 H]NE释放的增强，但不能阻断H2 O2（300μM）引起的电诱发[3 H]NE释放的增强。Tx合成酶抑制剂羧庚基咪唑（10μM）阻止E2-IsoP对诱发[3 H]NE释放的刺激作用，而不影响H2 O2诱导的反应。我们的结论是，IsoP的可以增强交感神经传递在牛离体虹膜，一种效果，可以通过Tx受体拮抗剂阻断。此外，内源性产生的Tx介导IsoP对NE释放的刺激作用。然而，内源性产生的IsoP或Tx不参与H2 O2诱导的交感神经传递增强。
Isoprostanes (IsoP) are formed by free radical catalyzed peroxidation of arachidonic acid independent of the cyclooxygenase enzyme. In the present study, we examined the effect of IsoP on norepinephrine (NE) release from the bovine isolated iris. Furthermore, we studied the role of IsoP's in hydrogen peroxide (H2O2)-induced enhancement of NE release from this tissue. Isolated bovine irides were prepared for studies of [3H]NE release using the superfusion method. Release of [3H]NE was induced via electrical field stimulation. Both 8-iso-prostaglandin E2(E2-IsoP) and 8-iso-prostaglandin F2α(F2-IsoP) produced a concentration-related enhancement of field-stimulated [3H]NE release from isolated bovine irides, an effect that was mimicked by the thromboxane (Tx) receptor agonist, U46619 and by H2O2. The Tx-receptor antagonist, SQ 29548 inhibited responses to E2-IsoP (10μM) with an IC50of 370±50 nM. SQ 29548 (10μM) also blocked the enhancement of electrically-evoked [3H]NE release induced by U46619 (10μM) but not that caused by H2O2(300μM). The Tx synthetase inhibitor, carboxyheptylimidazole (10μM) prevented the stimulatory effect of E2-IsoP on evoked [3H]NE release without affecting responses induced by H2O2. We conclude that IsoP's can enhance sympathetic neurotransmission in the bovine isolated iris, an effect that can be blocked by a Tx-receptor antagonist. Furthermore, endogenously produced Tx's mediate the stimulatory effect of IsoP's on NE release. However, endogenously generated IsoP's or Tx's are not involved in H2O2-induced potentiation of sympathetic neurotransmission.