Cardiac Fibrosis Sample Clauses

Cardiac Fibrosis. 1.3.3.1 The role of RAS Fibrosis is multifactorial and can result from a variety of causes including myocardial ischaemia, senescence, diabetes and hormones such as AngII amongst other causes. It is common to identify two different types of fibrosis, namely, reparative and reactive fibrosis. Reparative fibrosis occurs as a reaction to a loss of myocardial tissue due to necrosis or apoptosis, and is mainly interstitial. In contrast, reactive fibrosis is observed in the absence of cell loss as a reaction to inflammation and is primarily perivascular (Swynghedauw, 1999). Such adverse remodelling of the heart’s non-muscular compartment in hypertension is not necessarily due to the mechanical pressure overload. In models of infra-renal aortic banding with normal circulating levels of AngII and aldosterone, there is no evidence of increased cardiac fibrosis despite the presence of significant hypertrophy (Xxxxxx et al., 1990). Similarly chronic elevation of noradrenaline levels is also not associated with increased cardiac fibrosis despite an elevation in blood pressure (Xxxxx et al., 1989). Furthermore in human hypertension, fibrosis has been found in both the left and right ventricles in biopsies of myocardial tissue, despite the right heart pumping blood against a reduced afterload, suggesting that humoral factors are more important than the mechanical loading in the bringing about the fibrotic response (Xxxxxxx et al., 1994). Raised levels of AngII are thought to play a key role in triggering the inflammatory response resulting in fibrosis. In support of this many studies have shown that the blockade of AngII or its action results in a reduction in fibrosis. For example Xxxxxx et al (Xxxxxx et al., 2004) demonstrated that a sub-depressor dose of candersartan (an angiotensin II receptor blocker) in mice who had had supra-renal aortic banding markedly ameliorated perivascular fibrosis. One of the ways AngII is thought to initiate fibrosis is by up-regulating the expression of macrophage chemoattractant protein-1 (MCP-1), which is a major regulator of macrophage recruitment into inflammatory tissues. It has been observed that pressure overloaded hearts show an increased expression of MCP-1 which was accompanied by macrophage infiltration in the perivascular space of both small and large intramyocardial arteries (Capers et al., 1997; Xxxxxx et al., 2004). Administration of sub-depressor dose of candesartan significantly suppressed MCP-1 induction and macrophage ...
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