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AT 1 receptor‐mediated stimulation by angiotensin II of rat aortic fibronectin gene expression in vivo
Author(s) -
Kim Shokei,
Ohta Kensuke,
Hamaguchi Akinori,
Omura Takashi,
Tominaga Kazunari,
Yukimura Tokihito,
Miura Katsuyuki,
Tanaka Motoharu,
Iwao Hiroshi
Publication year - 1994
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1994.tb17042.x
Subject(s) - angiotensin ii , endocrinology , medicine , hydralazine , fibronectin , renin–angiotensin system , receptor , receptor antagonist , in vivo , antagonist , blood pressure , chemistry , stimulation , angiotensin receptor , biology , biochemistry , cell , microbiology and biotechnology
Fibronectin plays an important role in various vascular diseases. A subpressor (200 ng kg −I min −1 ) or pressor (1000 ng kg −1 min −1 ) dose of angiotensin II was continuously infused into rats by osmotic minipump for various times, to investigate the effects on aortic fibronectin gene expression. In rats infused with a subpressor dose of angiotensin II in which blood pressure was normal for 3 days, aortic fibronectin mRNA levels started to increase by 1.4 fold at 12 h and reached the maximal levels (increased by 3.1 fold) at 3 days. Treatment with TCV‐116 (3 mg kg −1 day −1 ), a non‐peptide selective AT 1 receptor antagonist, completely inhibited the angiotensin II‐induced increase in aortic fibronectin mRNA, while hydralazine (10 mg kg −1 day −1 ) did not block this effect. Similar results were also obtained for a pressor dose of angiotensin II. Thus, angiotensin II directly stimulates aortic fibronectin gene expression in vivo , which is mediated by the AT 1 receptor but not by blood pressure.