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首页> 美国卫生研究院文献>American Journal of Physiology - Heart and Circulatory Physiology >Soluble epoxide hydrolase-dependent regulation of myogenic response and blood pressure
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Soluble epoxide hydrolase-dependent regulation of myogenic response and blood pressure

机译：可溶性环氧化物水解酶对肌反应和血压的依赖性调节

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Epoxyeicosatrienoic acids (EETs) are metabolites of arachidonic acid via cytochrome P450 (CYP)/epoxygenases. EETs possess cardioprotective properties and are catalyzed by soluble epoxide hydrolase (sEH) to dihydroxyeicosatrienoic acids (DHETs) that lack vasoactive property. To date, the role of sEH in the regulation of myogenic response of resistant arteries, a key player in the control of blood pressure, remains unknown. To this end, experiments were conducted on sEH-knockout (KO) mice, wild-type (WT) mice, and endothelial nitric oxide synthase (eNOS)-KO mice treated with t-TUCB, a sEH inhibitor, for 4 wk. sEH-KO and t-TUCB-treated mice displayed significantly lower blood pressure, associated with significantly increased vascular EETs and ratio of EETs/DHETs. Pressure-diameter relationships were assessed in isolated and cannulated gracilis muscle arterioles. All arterioles constricted in response to increases in transmural pressure from 60 to 140 mmHg. The myogenic constriction was significantly reduced, expressed as an upward shift of pressure-diameter curve, in arterioles of sEH-KO and t-TUCB-treated eNOS-KO mice compared with their controls. Removal of the endothelium, or treatment of the vessels with PPOH, an inhibitor of EET synthase, restored the attenuated pressure-induced constriction to the levels similar to those observed in their controls but had no effects on control vessels. No difference was observed in the myogenic index, or in the vascular expression of eNOS, CYP2C29 (EET synthase), and CYP4A (20-HETE synthase) among these groups of mice. In conclusion, the increased EET bioavailability, as a function of deficiency/inhibition of sEH, potentiates vasodilator responses that counteract pressure-induced vasoconstriction to lower blood pressure.
机译：环氧二十碳三烯酸（EET）是花生四烯酸通过细胞色素P450（CYP）/环氧酶的代谢产物。 EET具有心脏保护性能，并通过可溶性环氧化物水解酶（sEH）催化形成缺乏血管活性的二羟基二十碳三烯酸（DHET）。迄今为止，sEH在调节抗性动脉的成肌反应中的作用仍是未知的，抗性动脉是控制血压的关键因素。为此，对用sEH抑制剂t-TUCB处理了4周的sEH敲除（KO）小鼠，野生型（WT）小鼠和内皮型一氧化氮合酶（eNOS）-KO小鼠进行了实验。 sEH-KO和t-TUCB处理的小鼠血压显着降低，与血管EET和EET / DHET比例显着增加有关。在孤立的和插管的鞭毛肌小动脉中评估压力-直径关系。响应于透壁压力从60 mmHg增加到140 mmHg，所有小动脉都收缩。与对照相比，在sEH-KO和t-TUCB处理的eNOS-KO小鼠的小动脉中，肌源性收缩明显降低，表现为压力-直径曲线的向上移动。去除内皮或用PPOH（EET合酶的抑制剂）处理血管，可使压力诱发的收缩恢复至与对照组相似的水平，但对对照组无影响。在这些小鼠组中，在肌原性指数或eNOS，CYP2C29（EET合酶）和CYP4A（20-HETE合酶）的血管表达方面均未观察到差异。总之，随着sEH缺乏/抑制，增加的EET生物利用度增强了血管舒张反应，从而抵消了压力引起的血管收缩以降低血压。

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