Poulat P, D'Orléans-Juste P, de Champlain J, Couture R
Department of Physiology, Faculty of Medicine, Université de Montréal, Québec, Canada.
J Cardiovasc Pharmacol. 1995;26 Suppl 3:S148-9.
In rat spinal cord slices, endothelin-1 (ET-1) and -3 (ET-3), sarafotoxin 6c (STX-6c), and the ETB receptor agonist IRL-1620 produced increases of [3H]inositol phosphate (IP) accumulation with the following rank order of potency: ET-1 > ET-3 >> STX-6c = IRL-1620. The ET-1- and ET-3-induced IP accumulations were blocked by BQ-123, a selective ETA antagonist, with a similar inhibition constant (IC50 16.7 +/- 3.4 microM and 8.0 +/- 1.6 microM, respectively) whereas BQ-788, a selective ETB antagonist, was inactive. These data indicate that ET-induced IP accumulation in rat spinal cord is mediated by an ETA receptor. The present study is in agreement with ETA receptor-mediated cardiovascular changes induced by intrathecal injection of ET-1 in the conscious rat.
在大鼠脊髓切片中，内皮素-1（ET-1）和-3（ET-3）、芋螺毒素6c（STX-6c）以及ETB受体激动剂IRL-1620均可使[3H]肌醇磷酸（IP）积累增加，其效力顺序如下：ET-1 > ET-3 >> STX-6c = IRL-1620。ET-1和ET-3诱导的IP积累被选择性ETA拮抗剂BQ-123阻断，抑制常数相似（IC50分别为16.7±3.4微摩尔和8.0±1.6微摩尔），而选择性ETB拮抗剂BQ-788则无活性。这些数据表明，ET诱导的大鼠脊髓IP积累是由ETA受体介导的。本研究与鞘内注射ET-1在清醒大鼠中诱导的ETA受体介导的心血管变化一致。
