内皮素ET（B）受体介导的兔基底动脉收缩

Endothelin ET(B) receptor-mediated constriction in the rabbit basilar artery.

作者信息

Zuccarello M, Boccaletti R, Rapoport R M

机构信息

Department of Neurosurgery, University of Cincinnati College of Medicine, Veterans Affairs Medical Center, OH 45267-0575, USA.

出版信息

Eur J Pharmacol. 1998 May 29;350(1):R7-9. doi: 10.1016/s0014-2999(98)00323-9.

DOI:10.1016/s0014-2999(98)00323-9

PMID:9683027

Abstract

The present study tests whether endothelin ET(B) receptor activation can mediate endothelin-1 constriction in the rabbit basilar artery in situ. Endothelin-1 (30 nM) induced 27% constriction of vessels pretreated with 1 microM BQ610 (homopiperidenyl-CO-Leu-DTrp (CHO)-D-Trp-OH), an endothelin ET(A) receptor antagonist, and the resulting constriction was completely relaxed by BQ788 (N-cis-2,6-dimethylpiperidinocarbonyl L-gamma-MeLeu-D-Trp (COOCH3)-Nle), an endothelin ET(B) receptor antagonist. Similarly, 30 nM endothelin-1 induced 30% constriction of vessels pretreated with 1 microM BQ788, and the resulting constriction was completely relaxed by BQ610. In contrast, sarafotoxin S6c, an endothelin ET(B) receptor agonist, did not induce constriction. This study suggests that in the basilar artery (1) endothelin ET(B) receptor activation can result in constriction and (2) the ability to elicit constriction is in some way dependent upon the agonist that activates the endothelin ET(B) receptor.

摘要

本研究检测内皮素ET(B)受体激活是否能介导原位兔基底动脉中内皮素-1的收缩作用。内皮素-1（30 nM）可使预先用1 μM BQ610（高哌啶基-CO-亮氨酸-D-色氨酸（CHO）-D-色氨酸-OH）（一种内皮素ET(A)受体拮抗剂）处理的血管收缩27%，而内皮素ET(B)受体拮抗剂BQ788（N-顺式-2,6-二甲基哌啶羰基-L-γ-甲基亮氨酸-D-色氨酸（COOCH3）-Nle）可使由此产生的收缩完全松弛。同样，30 nM内皮素-1可使预先用1 μM BQ788处理的血管收缩30%，而由此产生的收缩可被BQ610完全松弛。相比之下，内皮素ET(B)受体激动剂沙拉毒素S6c并未诱导血管收缩。本研究表明，在基底动脉中：(1) 内皮素ET(B)受体激活可导致血管收缩；(2) 引发血管收缩的能力在某种程度上取决于激活内皮素ET(B)受体的激动剂。