Staszewka-Barczak J, Ferreira S H, Vane J R
Cardiovasc Res. 1976 May;10(3):314-27. doi: 10.1093/cvr/10.3.314.
Application of bradykinin to the exposed ventricular surface of the dog heart elicits a reflex cardiovascular response which includes a rise in blood pressure, tachycardia, renal vasoconstriction and muscular vasodilation. The reflex response depends on the dose of bradykinin and is increased by concomitant application of prostaglandin E1 or E2 and reduced by indomethacin. Temporary occlusion of the coronary artery supplying the area of the ventricle under study also sensitized the heart to topical application of bradykinin. Bradykinin and prostaglandins are released by the heart during ischaemia. We suggest, therefore, that bradykinin and prostaglandins acting in concert are the natural stimulus for excitation of the sensory receptors signalling the pain of myocardial ischaemia. We also suggest that the nervous reflex which arises from activation of sympathetic sensory nerve endings is the mechanism subserving the cardiovascular events which accompany anginal attacks.
将缓激肽应用于犬心暴露的心室表面会引发一种反射性心血管反应，包括血压升高、心动过速、肾血管收缩和肌肉血管舒张。这种反射反应取决于缓激肽的剂量，同时应用前列腺素E1或E2会增强该反应，而消炎痛会减弱该反应。暂时阻断供应所研究心室区域的冠状动脉也会使心脏对局部应用缓激肽更加敏感。缓激肽和前列腺素在心肌缺血时由心脏释放。因此，我们认为，协同作用的缓激肽和前列腺素是激发感觉受体发出心肌缺血疼痛信号的天然刺激物。我们还认为，由交感感觉神经末梢激活引起的神经反射是伴随心绞痛发作的心血管事件的发生机制。
