缓激肽诱导冠状动脉舒张的机制及调节
Mechanism and modification of bradykinin-induced coronary vasodilation.
作者信息
Needleman P, Key S L, Denny S E, Isakson P C, Marshall G R
出版信息
Proc Natl Acad Sci U S A. 1975 Jun;72(6):2060-3. doi: 10.1073/pnas.72.6.2060.
Abstract
In isolated perfused rabbit hearts, bradykinin produced a concentration-dependent decrease in coronary resistance directly associated with biosynthesis and release of prostaglandin-E-like substance. An inhibitor of bradykinin destruction (the nonapeptide SQ-20881) markedly enhanced both the coronary vasodilation and release of prostaglandin-E-like substance produced by cardiac injection of bradykinin. Indomethacin inhibited both the myocardial prostaglandin biosynthesis and the decrease in coronary resistance induced by bradykinin. The demonstration that bradykinin is a potent stimulator of prostaglandin biosynthesis in the heart has implications as to the cause of the afferent cardiovascular reflexes and pain in myocardial infarction and angina pectoris.
摘要
在离体灌注兔心脏中，缓激肽可使冠状动脉阻力呈浓度依赖性降低，这与前列腺素E样物质的生物合成和释放直接相关。缓激肽破坏抑制剂（九肽SQ - 20881）显著增强了心脏注射缓激肽所产生的冠状动脉舒张作用以及前列腺素E样物质的释放。吲哚美辛抑制心肌前列腺素生物合成以及缓激肽诱导的冠状动脉阻力降低。缓激肽是心脏中前列腺素生物合成的有效刺激物这一发现，对心肌梗死和心绞痛时传入性心血管反射及疼痛的原因具有启示意义。
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