These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Does blockade of endothelinB1-receptor activation increase endothelinB2/endothelinA receptor-mediated constriction in the rabbit basilar artery?
    Author: Zuccarello M, Boccaletti R, Rapoport RM.
    Journal: J Cardiovasc Pharmacol; 1999 May; 33(5):679-84. PubMed ID: 10226852.
    Abstract:
    The purpose of this study was to investigate whether endothelin (ET)-1 activation of ETB1 receptors influences the relative magnitude of ETA/ETB2 receptor-mediated ET-1 constriction in the rabbit basilar artery. Initial challenge of ET-1-constricted vessels with BQ610, an ETA-receptor antagonist, resulted in approximately 60% relaxation, and subsequent addition of BQ788, an ETB1/2-receptor antagonist, relaxed the remaining constriction. To test whether blockade of ETB1 receptors influenced the relative magnitude of ETA/ETB2 receptor-mediated constriction, ET-1-constricted vessels were exposed to RES-701-1, an ETB1-receptor antagonist, before challenge with BQ610 or BQ788. RES-701-1 enhanced the ET-1 constriction by approximately 60%, consistent with blockade of ETB1 receptor-mediated endothelium-dependent relaxation. In ET-1-constricted vessels treated with RES-701-1, BQ610 challenge resulted in complete relaxation, whereas BQ788 was without effect. However, when 10 nM acetylcholine was added to RES-701-1-treated ET-1-constricted vessels, (a) BQ610 challenge resulted in only approximately 30% relaxation, and subsequent BQ788 addition relaxed the remaining constriction; and (b) BQ788 challenge resulted in approximately 35% relaxation, and subsequent BQ610 addition relaxed the remaining constriction. Acetylcholine induced approximately 10% relaxation of RES-701-1-treated ET-1-constricted vessels. It is speculated that a dynamic relation exists between ETA and ETB2 receptor-mediated constriction, such that ET-1-induced ETB2 receptor-mediated constriction of the basilar artery is dependent on ETB1 receptor activation and, in the absence of this activation, the constriction reverts to completely ETA receptor mediated.
    [Abstract] [Full Text] [Related] [New Search]