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

Sassan Hafizi; A. Chester; M. Yacoub

doi:10.1016/j.peptides.2004.03.011

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

Sassan Hafizi, A. Chester, M. Yacoub

Research output: Contribution to journal › Article › peer-review

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 AT1 receptor antagonist losartan but not the AT2 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 AT1 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.

Original language	English
Pages (from-to)	1031-1033
Number of pages	3
Journal	Peptides
Volume	25
Issue number	6
DOIs	https://doi.org/10.1016/j.peptides.2004.03.011
Publication status	Published - Jun 2004

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title = "Differential response of human cardiac fibroblasts to angiotensin I and angiotensin II",

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 AT1 receptor antagonist losartan but not the AT2 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 AT1 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.",

author = "Sassan Hafizi and A. Chester and M. Yacoub",

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T1 - Differential response of human cardiac fibroblasts to angiotensin I and angiotensin II

AU - Hafizi, Sassan

AU - Chester, A.

AU - Yacoub, M.

PY - 2004/6

Y1 - 2004/6

N2 - 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 AT1 receptor antagonist losartan but not the AT2 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 AT1 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.

AB - 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 AT1 receptor antagonist losartan but not the AT2 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 AT1 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.

U2 - 10.1016/j.peptides.2004.03.011

DO - 10.1016/j.peptides.2004.03.011

M3 - Article

SN - 0196-9781

VL - 25

SP - 1031

EP - 1033

JO - Peptides

JF - Peptides

IS - 6

ER -

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

Abstract

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