cGMP mediates the desensitization to bradykinin in isolated canine coronary arteries.
cGMP mediates the desensitization to bradykinin in isolated canine coronary arteries.
复制标题
cGMP 介导离体犬冠状动脉对缓激肽的脱敏。
DOI：
10.1152/ajpheart.1995.268.2.h865
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发表时间：
1995
期刊：
影响因子：
--
通讯作者：
Vanhoutte,PM
中科院分区：
文献类型：
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作者：
Olmos,L;Mombouli,JV;Illiano,S;Vanhoutte,PM
犬冠状动脉中缓激肽的松弛是由内皮源性一氧化氮（NO）和超极化因子（EDHF）介导的。通过将具有内皮的犬冠状动脉与10(-8)M缓激肽一起温育30分钟来诱导对激肽的脱敏。冲洗后，用前列腺素F2α使组织收缩，并在用吲哚美辛处理的对照动脉和脱敏动脉中获得缓激肽的浓度-松弛曲线。脱敏后，缓激肽的浓度-松弛曲线向右移动。然而，缓激肽引起的 3',5'-环磷酸鸟苷 (cGMP) 水平升高在两组组织中相似。在 NG-硝基-L-精氨酸（一种 NO 合酶抑制剂）存在下获得的缓激肽曲线下降，而在用钾收缩的动脉中获得的缓激肽曲线（以消除 EDHF 介导的松弛）则不受脱敏的影响。在脱敏程序之前添加 NG-硝基-L-精氨酸、氧合血红蛋白或亚甲蓝可以保留，而 3-吗啉代亚胺（SIN-1，NO 供体）和 8-溴鸟苷 3',5'-环单磷酸会损害 EDHF 介导的缓激肽松弛。因此，EDHF 依赖性缓激肽松弛的选择性损害可能是由 NO 介导的，主要通过增加 cGMP 的产生来发挥作用。
The relaxation to bradykinin in canine coronary arteries is mediated by endothelium-derived nitric oxide (NO) and hyperpolarizing factor (EDHF). Desensitization to the kinin was induced by incubation of canine coronary arteries with endothelium with 10(-8) M bradykinin for 30 min. After washout, tissues were contracted with prostaglandin F2 alpha, and concentration-relaxation curves to bradykinin were obtained in control and desensitized arteries treated with indomethacin. After desensitization, there was a shift to the right of the concentration-relaxation curves to bradykinin. However, the elevation in guanosine 3',5'-cyclic monophosphate (cGMP) levels evoked by bradykinin was similar in both groups of tissues. The curves to bradykinin obtained in the presence of NG-nitro-L-arginine (an NO synthase inhibitor) were depressed, whereas those obtained in arteries contracted with potassium (to eliminate the EDHF-mediated relaxation) were not affected by the desensitization. Addition of NG-nitro-L-arginine, oxyhemoglobin, or methylene blue before the desensitization procedure preserved, whereas 3-morpholinosydnonimine (SIN-1, a donor of NO) and 8-bromoguanosine 3',5'-cyclic monophosphate impaired, the EDHF-mediated relaxation to bradykinin. Thus the selective impairment of the EDHF-dependent relaxation to bradykinin may be mediated by NO, acting mainly through increased production of cGMP.