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Differential response of human cardiac fibroblasts to angiotensin I and angiotensin II

Hafizi, Sassan LU ; Chester, AH and Yacoub, MH (2004) In Peptides 25(6). p.1031-1033
Abstract
The vasoactive peptide angiotensin II (Ang II) has been implicated as a mediator of myocardial fibrosis. We carried out a comparative investigation of the effects of Ang II and its precursor Ang I on collagen metabolism and proliferation in cultured human cardiac fibroblasts. Cardiac fibroblasts responded to both Ang I and Ang II with concentration-dependent increases in collagen synthesis but no proliferation. The stimulatory effect of Ang II was abolished by the AT, receptor antagonist losartan but not the AT(2) receptor antagonist PD123319. The response to Ang I was not affected by either antagonist, nor by the angiotensin-converting enzyme (ACE) inhibitor captopril. In conclusion, Both Ang I and Ang II stimulate collagen synthesis of... (More)
The vasoactive peptide angiotensin II (Ang II) has been implicated as a mediator of myocardial fibrosis. We carried out a comparative investigation of the effects of Ang II and its precursor Ang I on collagen metabolism and proliferation in cultured human cardiac fibroblasts. Cardiac fibroblasts responded to both Ang I and Ang II with concentration-dependent increases in collagen synthesis but no proliferation. The stimulatory effect of Ang II was abolished by the AT, receptor antagonist losartan but not the AT(2) receptor antagonist PD123319. The response to Ang I was not affected by either antagonist, nor by the angiotensin-converting enzyme (ACE) inhibitor captopril. In conclusion, Both Ang I and Ang II stimulate collagen synthesis of human cardiac fibroblasts, the effect of Ang II occurring via the AT, receptor whilst Ang I appears to exert a direct effect through non-Ang II-dependent mechanisms. These results suggest distinct roles for angiotensin peptides in the development of cardiac fibrosis. (C) 2004 Elsevier Inc. All rights reserved. (Less)
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author
; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
collagen, fibroblast, cardiac, human, angiotensin, receptors
in
Peptides
volume
25
issue
6
pages
1031 - 1033
publisher
Elsevier
external identifiers
  • pmid:15203251
  • wos:000222395900017
  • scopus:2942593927
  • pmid:15203251
ISSN
1873-5169
DOI
10.1016/j.peptides.2004.03.011
language
English
LU publication?
yes
id
ea95182d-0b35-4d51-be1f-e6edd40026ca (old id 273438)
date added to LUP
2016-04-01 12:25:34
date last changed
2022-01-27 03:33:01
@article{ea95182d-0b35-4d51-be1f-e6edd40026ca,
  abstract     = {{The vasoactive peptide angiotensin II (Ang II) has been implicated as a mediator of myocardial fibrosis. We carried out a comparative investigation of the effects of Ang II and its precursor Ang I on collagen metabolism and proliferation in cultured human cardiac fibroblasts. Cardiac fibroblasts responded to both Ang I and Ang II with concentration-dependent increases in collagen synthesis but no proliferation. The stimulatory effect of Ang II was abolished by the AT, receptor antagonist losartan but not the AT(2) receptor antagonist PD123319. The response to Ang I was not affected by either antagonist, nor by the angiotensin-converting enzyme (ACE) inhibitor captopril. In conclusion, Both Ang I and Ang II stimulate collagen synthesis of human cardiac fibroblasts, the effect of Ang II occurring via the AT, receptor whilst Ang I appears to exert a direct effect through non-Ang II-dependent mechanisms. These results suggest distinct roles for angiotensin peptides in the development of cardiac fibrosis. (C) 2004 Elsevier Inc. All rights reserved.}},
  author       = {{Hafizi, Sassan and Chester, AH and Yacoub, MH}},
  issn         = {{1873-5169}},
  keywords     = {{collagen; fibroblast; cardiac; human; angiotensin; receptors}},
  language     = {{eng}},
  number       = {{6}},
  pages        = {{1031--1033}},
  publisher    = {{Elsevier}},
  series       = {{Peptides}},
  title        = {{Differential response of human cardiac fibroblasts to angiotensin I and angiotensin II}},
  url          = {{http://dx.doi.org/10.1016/j.peptides.2004.03.011}},
  doi          = {{10.1016/j.peptides.2004.03.011}},
  volume       = {{25}},
  year         = {{2004}},
}