Volume 3, Number 3, September 2002

Stimulation of collagen gel contraction by angiotensin II and III in cardiac fibroblasts
Paul Lijnen, Victor Petrov, Kandelaria Rumilla, Robert Fagard

Objective: The aim of the present study was to investigate whether angiotensin II (Ang II), angiotensin III (Ang III) or Ang II (2-8), angiotensin IV (Ang IV) or Ang II (3-8) and Ang II (1-7), Ang II (4-8), Ang II (5-8) and Ang II (1-4) can stimulate collagen gel contraction in cardiac fibroblasts in serum-free conditions.
Methods: Cardiac fibroblasts (from male adult Wistar rats) from passage 2 were cultured to confluency and added to a hydrated collagen gel in a Dulbecco's Modified Eagle's Medium, with or without foetal bovine serum, for one, two or three days. The area of the collagen gels embedded with cardiac fibroblasts was determined by a densitometric analysis. Collagen gel contraction was characterised by a decrease in the gel area.
Results: Ang II dose-dependently stimulated the contraction of collagen mediated by cardiac fibroblasts after one, two or three days of incubation in a serum-free medium. Telmisartan completely blocked the Ang II-induced collagen contraction by cardiac fibroblasts.
PD 123319 and des-Asp¹-Ile⁸-Ang II had no effect on the Ang II-induced collagen contraction by cardiac fibroblasts. Ang III also stimulated the contraction of collagen mediated by cardiac fibroblasts after one, two or three days of incubation in a serum-free medium. des-Asp¹-Ile⁸-Ang II and telmisartan completely blocked the Ang III-induced collagen gel contraction by cardiac fibroblasts. des-Asp¹-Ile⁸-Ang II, however, had no effect on the Ang II-induced collagen gel contraction by cardiac fibroblasts. Ang IV and Ang II (4-8), (5-8), (1-7) and (1-4), however, had no effect on collagen gel contraction by cardiac fibroblasts. Addition of telmisartan, PD 123319 or des-Asp¹-Ile⁸-Ang II alone did not affect collagen gel contraction by cardiac fibroblasts.
Conclusion: Our data demonstrate that the effects of Ang II on the collagen gel contraction by adult rat cardiac fibroblasts in serum-free conditions are Ang II type 1(AT₁)-receptor- mediated, because they are abolished by the specific AT₁-receptor antagonist, telmisartan, and not by the AT₂-receptor antagonist PD 123319 or by the Ang III antagonist des-Asp¹-Ile⁸-angiotensin. The Ang III- stimulated contraction of collagen by cardiac fibroblasts is completely blocked by the Ang III receptor antagonist, des-Asp¹-Ile⁸-angiotensin II, and by telmisartan.

JRAAS 2002;3:160-166.

View full PDF article (open in new window)
Email this article

Right click on this DOI link and copy link to cite this article (What is a DOI link?)