Handa R K, Strandhoy J W, Buckalew V M
Department of Medicine/Nephrology and Physiology and Pharmacology, Bowman Gray School of Medicine, Wake Forest University, Winston-Salem, North Carolina 27157.
Am J Physiol. 1991 Jul;261(1 Pt 2):F108-16. doi: 10.1152/ajprenal.1991.261.1.F108.
We examined the effect of platelet-activating factor (PAF) on renal vascular reactivity in the pentobarbital sodium-anesthetized male Wistar rat. Intrarenal infusion of C16-PAF at hypotensive (2.5 ng.min-1.kg-1) or nonhypotensive (0.5 ng.min-1.kg-1) doses caused renal vasodilation and dose dependently antagonized the renal vasoconstrictor responses of intrarenal boluses of angiotensin II (ANG II) greater than norepinephrine (NE) greater than vasopressin (AVP). PAF infusion at the high dose did not alter non-receptor-mediated renal vasoconstriction induced by intrarenal KCl injection. The inhibitory effect of PAF on agonist-induced renal vasoconstriction was accentuated by eicosanoid synthesis inhibition (indomethacin or dexamethasone), unaffected by dopamine-receptor blockade (haloperidol) but was totally abolished by PAF receptor antagonism (L-659,989). In contrast, intrarenal infusion of a calcium channel antagonist (nimodipine) or an intracellular calcium channel antagonist (TMB-8) equally inhibited the renal vasoconstrictor responses of ANG II, NE, and AVP. Thus PAF can cause renal vasodilation in the rat kidney and dose-dependently antagonizes the renal vasoconstrictor responses of ANG II greater than NE greater than AVP. The inhibitory effect of PAF on renal vasoconstrictor responses is mediated by PAF receptors and does not appear to be due to a nonspecific membrane effect, reduction in calcium mobilization, or the release of vasodilatory eicosanoids or dopamine.
我们研究了血小板活化因子（PAF）对戊巴比妥钠麻醉的雄性Wistar大鼠肾血管反应性的影响。在低血压剂量（2.5 ng·min⁻¹·kg⁻¹）或非低血压剂量（0.5 ng·min⁻¹·kg⁻¹）下肾内输注C16 - PAF可引起肾血管舒张，并剂量依赖性地拮抗肾内注射血管紧张素II（ANG II）、去甲肾上腺素（NE）、血管加压素（AVP）推注所引起的肾血管收缩反应，其中ANG II的作用大于NE，NE大于AVP。高剂量PAF输注并未改变肾内注射氯化钾诱导的非受体介导的肾血管收缩。PAF对激动剂诱导的肾血管收缩的抑制作用在抑制类花生酸合成（吲哚美辛或地塞米松）时增强，不受多巴胺受体阻断（氟哌啶醇）影响，但被PAF受体拮抗剂（L - 659,989）完全消除。相比之下，肾内输注钙通道拮抗剂（尼莫地平）或细胞内钙通道拮抗剂（TMB - 8）同样抑制ANG II、NE和AVP的肾血管收缩反应。因此，PAF可引起大鼠肾脏血管舒张，并剂量依赖性地拮抗ANG II大于NE大于AVP的肾血管收缩反应。PAF对肾血管收缩反应的抑制作用由PAF受体介导，似乎并非由于非特异性膜效应、钙动员减少、血管舒张类花生酸或多巴胺释放所致。
