Handa R K, Strandhoy J W, Buckalew V M
Department of Medicine/Nephrology, Wake Forest University Medical Center Winston-Salem, North Carolina 27157.
Life Sci. 1991;49(10):747-52. doi: 10.1016/0024-3205(91)90107-m.
The renal vasoactive and systemic hypotensive effects of platelet activating factor (C16:0-PAF and C18:1-PAF) were examined in anesthetized male Wistar rats. Bolus injections of C16-PAF (0.5-25 ng/kg) and C18-PAF (2.5-200 ng/kg) into the arterial circulation of the kidney produced increases in renal blood flow (6-15%) before causing dose-dependent systemic hypotension (2-64 mmHg). The dose-response curves for renal blood flow and systemic blood pressure generated by intrarenal C18-PAF administration were approximately 7 fold to the right of the dose-response curves generated by C16-DPAF. Intrarenal injections of vehicle or the biologically inactive enantiomer C16-DPAF (25-200 ng/kg) did not affect renal blood flow or systemic blood pressure. These results suggest that C16:0-PAF is a more potent renal vasodilator and hypotensive lipid than C18:1-PAF.
在麻醉的雄性Wistar大鼠中检测了血小板活化因子（C16:0-PAF和C18:1-PAF）对肾血管活性和全身血压的影响。向肾脏动脉循环中推注C16-PAF（0.5 - 25 ng/kg）和C18-PAF（2.5 - 200 ng/kg）会使肾血流量增加（6 - 15%），然后才引起剂量依赖性的全身低血压（2 - 64 mmHg）。肾内注射C18-PAF所产生的肾血流量和全身血压的剂量反应曲线比C16-DPAF所产生的剂量反应曲线大约右移7倍。肾内注射溶剂或无生物活性的对映体C16-DPAF（25 - 200 ng/kg）不会影响肾血流量或全身血压。这些结果表明，与C18:1-PAF相比，C16:0-PAF是一种更强效的肾血管扩张剂和降压脂质。
