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利用卒中型自发性高血压大鼠（SHRsp）与正常血压对照Wistar－Kyoto大鼠（WKY）的胸主动脉螺旋条，研究了基础EDRF对α1激动剂本肾上腺素（PE）引起的血管收缩的影响。结果发现：（1）不论在SHRsp还是WKY，血管内皮的存在明显抑制PE引起的血管收缩，表现为收缩幅度减小，EC50加大。（2）不论是去内皮条还是有内皮条，其收组反应在SHRsp与WKY间无显著差异。（3）在WKY，10－5mol／L，10－4mol／L的左旋硝基精氨酸（L－NNA，一氧化氮合成酶抑制剂）或3．3×10－4mol／L的还原型血红蛋白（HbO2，EDRF灭活剂）均可使有内皮条的收缩达到去内皮条的水平。（4）在SHRsp，10－5mol／L的L－NNA与3．3×10－6mol／LHbO2虽增强有皮条的收缩，但并不能使其达到去皮条的水平。10－4mol／L的L－NNA也只能使有内皮条的收缩幅度达到去皮条的水平。本实验结果表明：（1）血管内皮细胞释放的基础EDRF调节α1激动剂引起的收缩反应。基础EDRF的作用可被内皮细胞NO合成酶的抑制剂或EDRF的清除剂所阻断，（2）在SHRsp，L－NNA与HbO2对PE引起的血管收缩的增强作用比在WKY弱，提示高血压时基础EDRF产生或作用的机制可能发生改变，由正常时完全依赖NO合成酶变为部分地不依赖NO合成酶。推测其原因为高血压时一种非NO性质的基础EDRF
The effects of basic EDRF on the vasoconstriction induced by the α1 agonist, epinephrine (PE), were studied using the thoracic aortic spire of a stroke-prone spontaneously hypertensive rat (SHRsp) and a normotensive control Wistar-Kyoto rat (WKY) influences. The results showed that: (1) Vascular endothelium significantly inhibited the vasoconstriction induced by PE in either SHRsp or WKY, showing a decrease of contraction amplitude and an increase of EC50. (2) No difference was found between SHRsp and WKY in either endothelium or endothelium. (3) In the WKY, 10-5mol / L, 10-4mol / L of L-NNA (L-NNA, nitric oxide synthase inhibitor) or 3.3 × 10-4mol / L of reduced Hemoglobin (HbO2, EDRF inactivator) can make the contraction of the endothelium reach the level of endothelium. (4) In SHRsp, 10-5mol / L L-NNA and 3.3 × 10-6mol / LHbO2 enhanced the contraction of the skin, but it did not reach the level of skinning. 10-4mol / L of L-NNA also only makes the contraction of endothelial stripping rate reached the level of skin. The experimental results show that: (1) The basic EDRF released by vascular endothelial cells regulates the contractile response induced by α1 agonists. The role of basal EDRF can be blocked by inhibitors of endothelial NO synthase or EDRF, (2) the enhanced effect of L-NNA and HbO2 on PE-induced vasoconstriction in SHRsp is weaker than in WKY, suggesting a high The underlying EDRF mechanism of production or effect may change when blood pressure is varied from being normally dependent on NO synthase to being partially independent of NO synthase. Speculated that the reason for hypertension is a non-NO nature of the basic EDRF