Greenberg S S, Peevy K, Tanaka T P
Department of Physiology, University of Medicine and Dentistry of New Jersey-New Jersey Medical School, Newark.
Am J Hypertens. 1991 May;4(5 Pt 1):464-7. doi: 10.1093/ajh/4.5.464.
Evidence is presented that bradykinin inhibits norepinephrine efflux from sympathetic nerves innervating canine mesenteric and pulmonary arteries, in part, by releasing endothelium-derived relaxing factor (EDRF) from the vascular endothelium. Moreover, in the absence of vascular endothelium, bradykinin also inhibits norepinephrine efflux from the sympathetic nerve terminals innervating these blood vessels. This inhibition is attenuated by canavanine and LNMMA, which inhibit the conversion of arginine to nitric oxide, and is enhanced after overnight incubation of blood vessels with arginine. In endothelium-rubbed blood vessels the inhibitory effect of bradykinin on norepinephrine efflux is enhanced by increasing extracellular calcium ion ([Ca2+]o) and attenuated by nitrendipine. We propose that bradykinin inhibits norepinephrine efflux by stimulating intraneuronal nitric oxide from arginine.
有证据表明，缓激肽可部分通过从血管内皮释放内皮衍生舒张因子（EDRF）来抑制去甲肾上腺素从支配犬肠系膜动脉和肺动脉的交感神经外流。此外，在没有血管内皮的情况下，缓激肽也能抑制去甲肾上腺素从支配这些血管的交感神经末梢外流。刀豆氨酸和L - 硝基精氨酸甲酯（LNMMA）可抑制精氨酸向一氧化氮的转化，从而减弱这种抑制作用；而血管用精氨酸过夜孵育后，这种抑制作用会增强。在内皮被擦除的血管中，增加细胞外钙离子浓度（[Ca2+]o）可增强缓激肽对去甲肾上腺素外流的抑制作用，而尼群地平则可减弱这种作用。我们认为，缓激肽通过刺激精氨酸生成神经元内一氧化氮来抑制去甲肾上腺素外流。
