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Vascular response of tumour and normal tissues to endothelin‐1 following antagonism of ETA and ETB receptors in anaesthetised rats
Author(s) -
Bell Katrina M.,
Prise Vivien E.,
Chaplin David J.,
Wordsworth Sheila,
Tozer Gillian M.
Publication year - 1997
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/(sici)1097-0215(19971009)73:2<283::aid-ijc20>3.0.co;2-f
Subject(s) - vasoconstriction , endothelin receptor , blood flow , endocrinology , endothelin 1 , antagonism , vascular resistance , medicine , receptor , antagonist , blood vessel , fibrosarcoma , chemistry , biology , hemodynamics , pathology
Modification of blood flow by endothelin‐1 (ET‐1) was examined in the s.c. HSN fibrosarcoma and compared to normal tissues of anaesthetised CBH/CBi rats. The ET receptor subtypes involved in the response were investigated using the ETA and ETB receptor antagonists BQ‐610 and BQ‐788, respectively. Blood flow and vascular resistance were determined using the uptake of radiolabelled iodo‐antipyrine ( 125 I‐IAP). BQ‐610 or BQ‐788 was infused for 30 min prior to blood flow determination. ET‐1 was administered 15 min into the infusion time. BQ‐610 and BQ‐788 infused alone did not modify any vascular parameters. Tumour blood flow increased slightly following ET‐1, contrasting with most normal tissues, in which blood flow was reduced. Vascular resistance increased in all tissues, including the tumour. Neither antagonist significantly modified the ET‐1‐induced changes in tumour blood flow or vascular resistance, whereas in the majority of normal tissues BQ‐610 attenuated and BQ‐788 potentiated the vascular resonse to ET‐1. Our results show that the HSN tumour vasculature is only weakly responsive to ET‐1 and antagonism of its effects by BQ‐610 and BQ‐788. This contrasts with the majority of normal tissues, in which ET‐1 induces an intense vasoconstriction. Int. J. Cancer 73:283–289, 1997. © 1997 Wiley‐Liss, Inc.