Onoue H, Kaito N, Tomii M, Tokudome S, Nakajima M, Abe T
Department of Neurosurgery, Jikei University School of Medicine, Tokyo, Japan.
Am J Physiol. 1994 Sep;267(3 Pt 2):H880-6. doi: 10.1152/ajpheart.1994.267.3.H880.
We examined the activities of bradykinin, substance P, and vasopressin in isolated human cerebral arteries to better understand humoral control of cerebrovascular tone. Basilar and middle cerebral arteries were isolated from human cadavers during autopsy, and isometric tension was measured in helical strips of the arteries. Both bradykinin and substance P relaxed strips of both arteries precontracted with prostaglandin F2 alpha to similar extents. The relaxations induced by both peptides were abolished by removal of the vascular endothelium and were markedly reduced by pretreatment with NG-nitro-L-arginine, an inhibitor of endothelium-derived relaxing factor. Treatment with indomethacin, a cyclooxygenase inhibitor, did not attenuate the relaxations. These results indicate that the responses of human cerebral arteries to bradykinin and substance P are mediated by endothelium-derived relaxing factor. In contrast, vasopressin primarily produced endothelium-independent contractions in human cerebral arteries. Contractions of basilar arteries induced by vasopressin were much less than those of middle cerebral arteries. Two of eighteen basilar arteries, but none of the middle cerebral arteries, responded to vasopressin with endothelium-dependent relaxation. This suggests that the function of vasopressin receptors differs in basilar and middle cerebral arteries.
我们检测了缓激肽、P物质和血管加压素在离体人脑动脉中的活性,以更好地了解脑血管张力的体液调节。在尸检过程中从人体尸体分离出基底动脉和大脑中动脉,并在动脉螺旋条中测量等长张力。缓激肽和P物质均可使预先用前列腺素F2α预收缩的两种动脉条产生相似程度的舒张。去除血管内皮可消除两种肽诱导的舒张,并用内皮源性舒张因子抑制剂NG-硝基-L-精氨酸预处理可使其明显减弱。用环氧化酶抑制剂吲哚美辛处理并未减弱舒张作用。这些结果表明,人脑动脉对缓激肽和P物质的反应是由内皮源性舒张因子介导的。相反,血管加压素主要在人脑动脉中产生不依赖内皮的收缩。血管加压素诱导的基底动脉收缩远小于大脑中动脉。18条基底动脉中有2条,但大脑中动脉均无,对血管加压素产生内皮依赖性舒张反应。这表明血管加压素受体在基底动脉和大脑中动脉中的功能不同。