Bradykinin dilates rat middle cerebral artery and its large branches via endothelial B2 receptors and release of nitric oxide |
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Authors: | C. Gö rlach,M. Wahl |
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Affiliation: | Department of Physiology, LMU Munich, 80336, Munich, Germany |
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Abstract: | Ring segments of rat middle cerebral artery (MCA) were prepared for measurement of isometric force and precontracted with 10−4 M uridine triphosphate (UTP). Concentration-effect curves (CEC) were constructed for bradykinin (BK, 10−8–10−5 M) in segments with functionally intect (E+) or denuded (E−) endothelium. E− segments did not dilate to BK. The BK receptor was characterized by application of specific B1 or B2 antagonists [des-Arg9-Leu8] BK (10−5 M) and [-Arg0-Hyp3-Thi5--Tic7-Oic8] BK (HOE140,3 × 10−7 M), respectively, or B1 agonist [des-Arg9] BK (10−8–10−4 M). Involvement of nitric oxide (NO) was tested with NG-nitro--arginine (LNNA, 10−4 M). BK induced concentration-dependent relaxation with a maximal effect (Emax) of 40.86 ± 1.50% at 10−6 M and a pD2 (−log10 EC50) of 6.818 ± 0.044. This relaxation could be prevented with HOE140 or LNNA, but was not influenced by [des-Arg9-Leu8] BK. [des-Arg9] BK did not induce any effect. These results demonstrate that BK induced relaxation via endothelial B2 receptors and release of NO in isolated rat MCA. |
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Keywords: | Bradykinin NO B2 receptor Cerebral circulation Rat Isolated middle cerebral artery |
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