Zou A P, Imig J D, Kaldunski M, Ortiz de Montellano P R, Sui Z, Roman R J
Department of Physiology, Medical College of Wisconsin, Milwaukee 53226.
Am J Physiol. 1994 Feb;266(2 Pt 2):F275-82. doi: 10.1152/ajprenal.1994.266.2.F275.
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.
本研究评估了花生四烯酸（AA）的内源性P - 450代谢产物在大鼠肾血流自身调节中的作用。当肾灌注压在150至100 mmHg之间变化时，全肾和皮质血流得到良好的自身调节。向肾动脉输注17 - 十八碳炔酸（17 - ODAY）（33 nmol/min）可使皮质和乳头血流分别增加12.6±2.5%和26.5±4.6%。输注17 - ODAY后，全肾和皮质血流的自身调节受到损害。肾内输注咪康唑（8 nmol/min）对全肾、皮质或乳头血流的自身调节没有影响。17 - ODAY（1 μM）在体外可使肾小动脉前微血管生成20 - 羟基二十碳四烯酸（20 - HETE）以及11,12 - 和14,15 - 环氧二十碳三烯酸（EETs）的量分别减少83.7±7.4%和89.0±4.9%。咪康唑（1 μM）可使EETs的生成减少86.4±5.7%，但对20 - HETE的生成没有影响。这些结果表明，AA的内源性P - 450代谢产物，尤其是20 - HETE，可能参与肾血流的自身调节。
