Dunn M J, Scharschmidt L A, Lianos E A, Konieczkowski M
Clin Physiol Biochem. 1984;2(2-3):91-100.
Renal glomeruli have cyclo-oxygenase and lipoxygenase enzymes which convert arachidonic acid to prostaglandins, thromboxane and 12-hydroxyeicosatetraenoic acid. Glomerular epithelial and mesangial cells, in culture, also synthesize these arachidonate products. Angiotensin and vasopressin contract mesangial cells and stimulate mesangial synthesis of PGE2. PGE2, in the glomerulus, antagonizes the actions of angiotensin on the mesangium and hence reduces angiotensin-mediated glomerular contraction. Glomerular immune injury (nephrotoxic serum nephritis) augments glomerular production of prostaglandins and thromboxane. Thromboxane reduces glomerular function and inhibition of thromboxane synthesis preserves glomerular filtration rate and renal plasma flow in this disease model. Spontaneously hypertensive rats also have enhanced glomerular prostaglandin and thromboxane synthesis. Although acute inhibition of thromboxane synthesis will vasodilate the hypertensive rat kidney, chronic inhibition does not reduce blood pressure or increase renal blood flow.
肾小球含有环氧化酶和脂氧化酶，可将花生四烯酸转化为前列腺素、血栓素和12-羟基二十碳四烯酸。培养的肾小球上皮细胞和系膜细胞也能合成这些花生四烯酸产物。血管紧张素和血管加压素可使系膜细胞收缩，并刺激系膜细胞合成前列腺素E2。在肾小球中，前列腺素E2可拮抗血管紧张素对系膜的作用，从而减少血管紧张素介导的肾小球收缩。肾小球免疫损伤（肾毒性血清肾炎）可增加肾小球前列腺素和血栓素的生成。血栓素会降低肾小球功能，在该疾病模型中，抑制血栓素合成可维持肾小球滤过率和肾血浆流量。自发性高血压大鼠的肾小球前列腺素和血栓素合成也会增强。虽然急性抑制血栓素合成会使高血压大鼠的肾脏血管舒张，但长期抑制并不能降低血压或增加肾血流量。
