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Role of ET‐B receptors in the cardiac contractile force effects of endothelin‐1
Author(s) -
Wince Leon C.
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.a802
Subject(s) - inotrope , endothelin receptor , medicine , endocrinology , agonist , receptor , stimulation , chemistry , endothelin 1 , endothelin 3 , endothelins
Myocardium of mammalian species contains two subtypes of endothelin (ET) receptors: ET A and ET B . However, their role in the contractile force effects of endothelin‐1 (ET‐1) in different cardiac regions is unclear. The purpose of this study was to investigate the role of ET B receptors in the inotropic effects of ET‐1 in isolated rat left atria (LA). The importance of nitric oxide (NO) in the positive inotropic effects (PIE) of ET‐1 and in responses to selective ET B receptor stimulation was also examined. LA were mounted in tissue baths and electrically stimulated (1 Hz). Inotropic responses to ET‐1 and IRL‐1620 (ET B agonist) were studied in the presence of BQ‐788 (ET B antagonist) and L‐NAME (NO synthase inhibitor). BQ‐788 (10 −6 M) caused a significant leftward shift of the concentration‐response (CR) curve for ET‐1 and significantly increased the maximal effect. In contrast, L‐NAME (10 −4 M) did not significantly impact the CR curve for ET‐1. IRL‐1620 produced a biphasic concentration‐related negative inotropic effect (NIE). Pretreatment with L‐NAME significantly attenuated the NIE of IRL‐1620 and unveiled a small PIE between 10–30 nM. These results suggest that the ET B receptor mediates a modulatory negative inotropic influence on the PIE of ET‐1 in LA. Also, the data indicate that responses to ET B receptor stimulation in this tissue are possibly both NO‐dependent and NO‐independent. Supported by OUCOM.