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实验在３４只乌拉坦麻醉的雄性Ｗｉｓｔａｒ大鼠上进行，以肾灌流压（ＰＰｋ）指标，观察皂角苷和酚妥拉明灌流肾动脉对延髓腹面升压区（ＶＳＭｐ）兴奋诱发的肾血流阻抗增加效应的影响。结果表明：（１）皂角苷灌流肾动脉几乎完全取消了电刺激ＶＳＭｐ诱发的ＰＰｋ增加效应；（２）在电刺激ＶＳＭｐ诱发的ＰＰｋ升高期间，肾静脉收集液回灌同体肾动脉可提升ＰＰｋ；（３）酚妥拉明灌流肾动脉后，可明显抑制电刺激ＶＳＭｐ及肾上腺素灌流肾动脉诱发的ＰＰｋ升高作用；但对电刺激ＶＳＭｐ诱发ＰＰｋ升高期间肾静脉收集液回灌肾动脉产生的提升ＰＰｋ作用没有影响。提示ＶＳＭｐ提升肾血流阻抗作用依赖于血管内皮的存在。ＶＳＭｐ兴奋时可产生一种由α受体介导的内度依赖性，非α受体激动剂类的收缩因子。
The experiment was performed on 34 male Wistar rats anesthetized with urethane. The renal perfusion pressure (PPK) was used to observe the effects of saponin and phentolamine perfusing renal artery on the excited renal blood of VSMp Effect of Flow Impedance Increase Effect. The results showed that: (1) The renal arteries infused with saponin glycosides almost completely abolished the effect of VSMp-induced increase of PPK; (2) During the increase of PPM induced by electrical stimulation of VSMp, the renal vein collected liquid renal artery can be increased PPK; (3) Phentolamine perfusion of renal artery, can significantly inhibit the electrical stimulation of VSMp and adrenergic perfusion of renal artery induced PPK increased; but VSMp-induced increase of PPk renal vein collected during reperfusion kidney Arteries produce no effect on PPk uptake. Tip VSMp enhance renal blood flow resistance depends on the existence of vascular endothelial. When excited, VSMp produces an α -receptor-mediated endogenous, non-α-agonist-like contraction factor.