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实验用３００～３５０ｇ雄性Ｗｉｓｔａｒ大鼠，氨基甲酸乙酯腹腔麻醉。电刺激或Ｌ－谷氨酸微量注射于切断双侧迷走神经的大鼠延髓腹面降压区（ＶＳＭｄ），在降压反应的同时，肾血管灌流压（ＰＰｋ）下降。ＰＰｋ的下降依赖于肾神经及肾血管内皮的完整性，并近似于特异性α＿２肾上腺素受体阻断剂育亨宾灌流肾血管的反应。实验表明，ＶＳＭｄ的兴奋通过抑制肾交感神经对肾血管的基础紧张性影响，该影响依赖血管内皮，内皮损毁后，ＶＳＭｄ降ＰＰｋ的效应被取消。
Experimental male 350 ~ 350g Wistar rats, urethane anesthesia. Microinjection of L-glutamic acid into the medulla oblongata area (VSMd) of rats with bilateral vagal denervation resulted in a decrease in renal vascular perfusion pressure (PPk). PPk decline depends on the integrity of the renal and renal vascular endothelium, and similar to the specific α_2 adrenergic receptor blocker yohimbine perfusion of renal blood vessels. Experiments show that the excitement of VSMd by inhibiting renal sympathetic tone on the basis of renal vascular tension, which depends on vascular endothelial, endothelial damage, VSMd down PPk effect was canceled.