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本文应用双标本微量生物测定法观察自发高血压大鼠（ＳＨＲ）及其常压对照（ＷＫＹ）大鼠肠系膜动脉Ａｃｈ内皮依赖性舒张（ＥＤＲ）的变化，并对其机制进行初步探讨，结果发现：ＳＨＲ的ＡｃｈＥＤＲ显著弱于ＷＫＹ者；鸟苷酸环化酶抑制剂美蓝（５×１０－５ｍｏｌ／Ｌ）可明显减弱ＳＨＲ与ＷｋＹ的ＡＣｈＥＤＲ，此时ＳＨＲ的舒张仍明显弱于ＷＫＹ。灌流消炎痛（５×１０－５ｍｏｌ／Ｌ）后，卒中易感型自发高血压大鼠（ＳＨＲｓｐ）的ＡｃｈＥＤＲ增强，ＷＫＹ的舒张反应几乎不变。此时ＳＨＲｓｐ与ＷＫＹ的肠系膜动脉的ＡｃｈＥＤＲ的差异消失。以上结果支持高血压的内脏血管ＥＤＲ减弱的结论，并且可以认为乙酰胆碱（Ａｃｈ）激发的血管内皮舒张因子（ＥＤＲＦ）通过ｃＧＭＰ环节的功能发生变化。以及血管内皮细胞释放的收缩因子（ＥＤＣＦ）增多是这一减弱的原因之一。
In this paper, double-labeled micro-bioassay was used to observe the changes of the endothelium-dependent endothelium-dependent relaxation (EDR) of mesenteric artery in spontaneously hypertensive rats (SHR) and its normal-pressure control (WKY) rats. : SHR AchEDR was significantly weaker than WKY; guanosine cyclase inhibitor methylene blue (5 × 10-5mol / L) significantly reduced AChEDR SHR and WkY, SHR relaxation was still significantly weaker than WKY. After perfusion of indomethacin (5 × 10-5 mol / L), the AchEDR of SHRsp increased and the relaxation of WKY almost unchanged. At this point, the difference in AchEDR between the SHRsp and WKY mesenteric arteries disappeared. These results support the conclusion that EDR decreases in visceral blood vessels of hypertensive patients and that acetylcholine (Ach) -stimulated vascular endothelial relaxing factor (EDRF) changes through the function of cGMP. And the increase of the release of the contraction factor of endothelial cells (EDCF) is one of the reasons for this decrease.