1994
DOI: 10.1172/jci117243
|View full text |Cite
|
Sign up to set email alerts
|

Characterization of angiotensin II receptors in cultured adult rat cardiac fibroblasts. Coupling to signaling systems and gene expression.

Abstract: Cardiac hypertrophy is largely due to cardiac fibroblast growth and increased synthesis of extracellular matrix. This study has investigated the contribution of the vasoactive hormone, angiotensin II, toward Invest. 1994Invest. . 93:2372Invest. -2378

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
1
1

Citation Types

8
109
0

Year Published

1998
1998
2015
2015

Publication Types

Select...
8
1

Relationship

0
9

Authors

Journals

citations
Cited by 225 publications
(117 citation statements)
references
References 45 publications
8
109
0
Order By: Relevance
“…33 Cultures of adult rat cardiac fibroblasts express AT 1 but not AT 2 receptors and angiotensin II-stimulated increase in [Ca ++ ] i and several growth-related metabolic events including c-fos gene expression and increased synthesis of DNA, RNA and protein and collagen type I synthesis were blocked by losartan. 34 In the experiments using cultured rat or human mesangial cells, losartan inhibited the angiotensin II-stimulated hypertrophy [35][36][37] and proliferation 36,37 of the mesangial cells. Similar results have been reported in the experiments using cultured vascular smooth muscle cells; namely, angiotensin II with or without PDGF or EGF stimulated the proliferation of cultured smooth muscle cells, which was inhibited by losartan [38][39][40] or candesartan.…”
Section: Discussionmentioning
confidence: 99%
“…33 Cultures of adult rat cardiac fibroblasts express AT 1 but not AT 2 receptors and angiotensin II-stimulated increase in [Ca ++ ] i and several growth-related metabolic events including c-fos gene expression and increased synthesis of DNA, RNA and protein and collagen type I synthesis were blocked by losartan. 34 In the experiments using cultured rat or human mesangial cells, losartan inhibited the angiotensin II-stimulated hypertrophy [35][36][37] and proliferation 36,37 of the mesangial cells. Similar results have been reported in the experiments using cultured vascular smooth muscle cells; namely, angiotensin II with or without PDGF or EGF stimulated the proliferation of cultured smooth muscle cells, which was inhibited by losartan [38][39][40] or candesartan.…”
Section: Discussionmentioning
confidence: 99%
“…26 Traditionally, the effect of RAAS on promoting atrial and ventricular arrhythmias is explained based on increased cardiac hypertrophy, fibrosis, and heterogeneity of the cardiac tissue. 27 Nevertheless, such a model fails to explain the observed reversal of the proarrhythmic effects upon treatment with ACEIs or ARBs, suggesting other electrophysiological effects of RAAS activation. RAAS has manifold effects on the cardiovascular system and various possible pathways have been proposed as the link underlying the relationship between RAAS and arrhythmias.…”
Section: Introductionmentioning
confidence: 99%
“…Cardiac fibroblasts are activated in response to hypertrophic stimuli, including AngII. [14][15][16][17] Furthermore, fibroblasts proliferate and increase the production of ECM proteins in response to AngII exposure in vitro. However, the in vivo data available to support this response to AngII is limited.…”
mentioning
confidence: 99%
“…However, the in vivo data available to support this response to AngII is limited. 1,[14][15][16][17] Finally, if myofibroblasts make up a component of the cells that accumulate in the myocardium after AngII exposure, their origin remains to be determined. Myofibroblasts can arise from the activation and proliferation of resident fibroblasts or from several different sources including endothelial-mesenchymal transitions and blood borne mesenchymal progenitor cells (referred to as fibrocytes).…”
mentioning
confidence: 99%