Roman Richard J
Department of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin 53226, USA.
Physiol Rev. 2002 Jan;82(1):131-85. doi: 10.1152/physrev.00021.2001.
Recent studies have indicated that arachidonic acid is primarily metabolized by cytochrome P-450 (CYP) enzymes in the brain, lung, kidney, and peripheral vasculature to 20-hydroxyeicosatetraenoic acid (20-HETE) and epoxyeicosatrienoic acids (EETs) and that these compounds play critical roles in the regulation of renal, pulmonary, and cardiac function and vascular tone. EETs are endothelium-derived vasodilators that hyperpolarize vascular smooth muscle (VSM) cells by activating K(+) channels. 20-HETE is a vasoconstrictor produced in VSM cells that reduces the open-state probability of Ca(2+)-activated K(+) channels. Inhibitors of the formation of 20-HETE block the myogenic response of renal, cerebral, and skeletal muscle arterioles in vitro and autoregulation of renal and cerebral blood flow in vivo. They also block tubuloglomerular feedback responses in vivo and the vasoconstrictor response to elevations in tissue PO(2) both in vivo and in vitro. The formation of 20-HETE in VSM is stimulated by angiotensin II and endothelin and is inhibited by nitric oxide (NO) and carbon monoxide (CO). Blockade of the formation of 20-HETE attenuates the vascular responses to angiotensin II, endothelin, norepinephrine, NO, and CO. In the kidney, EETs and 20-HETE are produced in the proximal tubule and the thick ascending loop of Henle. They regulate Na(+) transport in these nephron segments. 20-HETE also contributes to the mitogenic effects of a variety of growth factors in VSM, renal epithelial, and mesangial cells. The production of EETs and 20-HETE is altered in experimental and genetic models of hypertension, diabetes, uremia, toxemia of pregnancy, and hepatorenal syndrome. Given the importance of this pathway in the control of cardiovascular function, it is likely that CYP metabolites of arachidonic acid contribute to the changes in renal function and vascular tone associated with some of these conditions and that drugs that modify the formation and/or actions of EETs and 20-HETE may have therapeutic benefits.
最近的研究表明,花生四烯酸在脑、肺、肾和外周血管系统中主要通过细胞色素P-450(CYP)酶代谢为20-羟基二十碳四烯酸(20-HETE)和环氧二十碳三烯酸(EETs),并且这些化合物在肾、肺和心脏功能以及血管张力的调节中发挥关键作用。EETs是内皮衍生的血管舒张剂,通过激活钾离子通道使血管平滑肌(VSM)细胞超极化。20-HETE是在VSM细胞中产生的血管收缩剂,它降低钙激活钾离子通道的开放状态概率。20-HETE形成的抑制剂在体外可阻断肾、脑和骨骼肌小动脉的肌源性反应以及体内肾和脑血流的自身调节。它们还可阻断体内的肾小管-肾小球反馈反应以及体内外组织PO₂升高时的血管收缩反应。血管平滑肌中20-HETE的形成受血管紧张素II和内皮素刺激,并受一氧化氮(NO)和一氧化碳(CO)抑制。阻断20-HETE的形成可减弱对血管紧张素II、内皮素、去甲肾上腺素、NO和CO的血管反应。在肾脏中,近端小管和髓袢升支粗段可产生EETs和20-HETE。它们调节这些肾单位节段中的钠离子转运。20-HETE还参与多种生长因子对VSM、肾上皮和系膜细胞的促有丝分裂作用。在高血压、糖尿病、尿毒症、妊娠毒血症和肝肾综合征的实验和遗传模型中,EETs和20-HETE的产生会发生改变。鉴于该途径在心血管功能控制中的重要性,花生四烯酸的CYP代谢产物可能导致与其中一些病症相关的肾功能和血管张力变化,并且调节EETs和20-HETE形成和/或作用的药物可能具有治疗益处。