Inhibition of renal vascular 20-HETE production impairs autoregulation of renal blood flow.
Inhibition of renal vascular 20-HETE production impairs autoregulation of renal blood flow.
复制标题
抑制肾血管 20-HETE 的产生会损害肾血流的自动调节。
DOI：
10.1152/ajprenal.1994.266.2.f275
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发表时间：
1994
期刊：
影响因子：
--
通讯作者：
Roman,RJ
中科院分区：
文献类型：
--
作者：
Zou,AP;Imig,JD;Kaldunski,M;OrtizdeMontellano,PR;Sui,Z;Roman,RJ
本研究探讨了内源性花生四烯酸（AA）代谢产物P-450对大鼠肾血流量自动调节的作用。当肾灌注压在150 ~ 100 mmHg范围内变化时，全肾和皮质血流自动调节良好。向肾动脉输注17-十八炔酸（17-ODYA）（33 nmol/min）分别使皮质和乳头状血管血流量增加12.6 +/-2.5%和26.5 +/-4.6%。17-ODYA后，全肾和皮质血流的自动调节受损。肾内输注咪康唑（8 nmol/min）对全肾、皮质或乳头状血流量的自动调节无影响。17-ODYA（1 μ M）在体外分别抑制肾小球前微血管20-羟基二十碳四烯酸（20-HETE）和11，12-和14，15-环氧二十碳三烯酸（E3）的形成83.7 +/- 7.4%和89.0 +/-4.9%。咪康唑（1 μ M）使Escherichia coli的形成减少了86.4 +/-5.7%，但对20-HETE的产生没有影响。这些结果表明，AA的内源性P-450代谢产物，特别是20-HETE，可能参与肾血流量的自动调节。
The present study evaluated the role of endogenous P-450 metabolites of arachidonic acid (AA) on autoregulation of renal blood flow in rats. Whole kidney and cortical blood flows were well autoregulated when renal perfusion pressure was varied from 150 to 100 mmHg. Infusion of 17-octadecynoic acid (17-ODYA) into the renal artery (33 nmol/min) increased cortical and papillary blood flows by 12.6 +/- 2.5 and 26.5 +/- 4.6%, respectively. After 17-ODYA, autoregulation of whole kidney and cortical blood flows was impaired. Intrarenal infusion of miconazole (8 nmol/min) had no effect on autoregulation of whole kidney, cortical, or papillary blood flows. 17-ODYA (1 microM) inhibited the formation of 20-hydroxyeicosatetraenoic acid (20-HETE) and 11,12- and 14,15-epoxyeicosatrienoic acids (EETs) by renal preglomerular microvessels in vitro by 83.7 +/- 7.4% and 89.0 +/- 4.9%, respectively. Miconazole (1 microM) reduced the formation of EETs by 86.4 +/- 5.7%, but it had no effect on the production of 20-HETE. These results suggest that endogenous P-450 metabolites of AA, particularly 20-HETE, may participate in the autoregulation of renal blood flow.