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Proceedings of the Symposium ‘Angiotensin AT 1 Receptors: From Molecular Physiology to Therapeutics’: CYTOKINES AND CARDIAC HYPERTROPHY: ROLES OF ANGIOTENSIN II AND BASIC FIBROBLAST GROWTH FACTOR
Author(s) -
Kaye David M,
Kelly Ralph A,
Smith Thomas W
Publication year - 1996
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.1996.tb03075.x
Subject(s) - autocrine signalling , angiotensin ii , paracrine signalling , angiotensin ii receptor type 1 , muscle hypertrophy , basic fibroblast growth factor , myocyte , growth factor , receptor , medicine , epidermal growth factor , endocrinology , biology , angiotensin receptor , fibroblast growth factor , microbiology and biotechnology
SUMMARY1 While the haemodynamic influences that cause cardiac hypertrophy are well known, the cellular and molecular mechanisms by which a mechanical stimulus is translated into a growth response by cardiac muscle have remained uncertain. 2 Current evidence suggests that a number of trophic factors may be released by cellular constituents of the heart, acting in an autocrine or paracrine manner to influence the growth response and phenotype of neighbouring cells. 3 Angiotensin II, acting via the AT 1 receptor subtype, and both basic fibroblast growth factor and heparin‐binding epidermal growth factor have been shown to exert hypertrophic actions in vivo and in vitro. Studies also indicate that cardiac myocytes themselves are capable of releasing all of these cytokines in response to increased mechanical load.