Tschudi M R, Lüscher T F
Department of Research, University Hospital Basel, Switzerland.
Biochem Biophys Res Commun. 1994 Oct 28;204(2):685-90. doi: 10.1006/bbrc.1994.2514.
Endothelin-1 (ET-1) and angiotensin II (AII) are potent vasoconstrictor hormones which regulate tissue perfusion and blood pressure. We pharmacologically characterized endothelin and angiotensin receptors mediating contractions of human mammary resistance arteries in myographs for isometric tension recording. ET-1 caused potent contractions. The concentration response curve was shifted to the right by ETA antagonist FR 139317, but a high sensitivity, low efficacy component remained. After incubation with ETB agonist sarafotoxin (S6c) this component of the concentration response curve resistant to FR 139317 disappeared. The ETA/ETB-receptor antagonist bosentan shifted the entire concentration response curve to the right. AI and AII caused marked contractions. The effects of AI were reduced by the ACE inhibitor benazeprilat, while those of AII were prevented by valsartan, an AT1 antagonist. In summary, in human resistance arteries, contractions to ET-1 are mediated by ETA- and ETB-receptors while those to AII are exclusively mediated by AT1-receptors.
内皮素-1（ET-1）和血管紧张素II（AII）是强效血管收缩激素，可调节组织灌注和血压。我们通过药理学方法对介导人体乳腺阻力动脉在肌张力记录肌动描记器中收缩的内皮素和血管紧张素受体进行了表征。ET-1引起强效收缩。ETA拮抗剂FR 139317使浓度-反应曲线右移，但仍保留一个高敏感性、低效能成分。在用ETB激动剂沙拉新（S6c）孵育后，浓度-反应曲线中对FR 139317耐药的这一成分消失。ETA/ETB受体拮抗剂波生坦使整个浓度-反应曲线右移。AI和AII引起明显收缩。ACE抑制剂贝那普利拉可降低AI的作用，而AT1拮抗剂缬沙坦可阻断AII的作用。总之，在人体阻力动脉中，ET-1引起的收缩由ETA和ETB受体介导，而AII引起的收缩仅由AT1受体介导。
