Handa R K, Strandhoy J W, Buckalew V M
Department of Medicine/Nephrology, Bowman Gray School of Medicine, Wake Forest University, Winston-Salem, North Carolina 27103.
Am J Physiol. 1990 Jun;258(6 Pt 2):F1504-9. doi: 10.1152/ajprenal.1990.258.6.F1504.
In view of the potent vasoactive properties of platelet-activating factor (PAF), we investigated the renal hemodynamic effects of this lipid. C16-PAF (0.5-10 ng/kg) given as a bolus into the renal arterial circulation of pentobarbital sodium-anesthetized male Wistar rats produced a dose-dependent increase in renal blood flow (6-15%), before causing systemic hypotension. The PAF-induced renal vasodilation and systemic hypotension was independent of renal innervation, unaltered by eicosanoid synthesis inhibition with indomethacin or dexamethasone, unchanged by the nonselective dopamine-receptor antagonist haloperidol, but was abolished by the PAF-receptor antagonist, L-659,989. Non-hypotensive intrarenal PAF infusion at 0.5 ng.min-1.kg-1 caused an increase in renal blood flow. Thus PAF can cause renal vasodilation in the rat kidney that is PAF-receptor mediated and does not involve the sympathetic nervous system or the release of vasodilatory arachidonic acid metabolites or dopamine.
鉴于血小板活化因子（PAF）具有强大的血管活性特性，我们研究了这种脂质对肾脏血流动力学的影响。在戊巴比妥钠麻醉的雄性Wistar大鼠的肾动脉循环中，一次性注射C16-PAF（0.5 - 10 ng/kg），在引起全身低血压之前，肾血流量呈剂量依赖性增加（6 - 15%）。PAF诱导的肾血管舒张和全身低血压与肾神经支配无关，吲哚美辛或地塞米松抑制类花生酸合成对其无影响，非选择性多巴胺受体拮抗剂氟哌啶醇对其无改变，但PAF受体拮抗剂L-659,989可消除这种作用。以0.5 ng·min-1·kg-1的剂量进行非低血压性肾内PAF输注可导致肾血流量增加。因此，PAF可在大鼠肾脏中引起肾血管舒张，这是由PAF受体介导的，不涉及交感神经系统，也不涉及血管舒张性花生四烯酸代谢产物或多巴胺的释放。
