Journal
HYPERTENSION RESEARCH
Volume 32, Issue 4, Pages 229-237Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/hr.2009.5
Keywords
organ damage; local RAS; oxidative stress; inflammation; fibroproliferative disease
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Funding
- Ministry of Education, Science, Sports, and Culture of Japan
- Takeda Science Foundation
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The renin-angiotensin system (RAS) is involved in the pathological mechanisms of target organ damage, as well as in the induction of hypertension. RAS inhibition by angiotensin converting enzyme (ACE) inhibitors and angiotensin (Ang) II receptor blockers can prevent tissue damage by inhibition of Ang II type 1 receptor signaling. A beneficial effect of RAS inhibition on the heart, vasculature and kidney in cardiovascular disease has been reported. However, RAS inhibition can also prevent fibroproliferative diseases and damage of other tissues, such as brain, adipose tissue and muscle, because local RAS has an important role in tissue damage compared with circulating RAS. Moreover, other players, such as Ang II type 2 receptor signaling, aldosterone and ACE2 have been highlighted. Furthermore, there has also been a focus on the emerging concept of regulation of RAS, such as receptor-interacting proteins and receptor modifications, in the new discovery of therapeutic agents for tissue protection. The RAS has a pivotal role in various target organ damage, with complicated mechanisms; therefore, blockade of RAS may be therapeutically effective in preventing organ damage, as well as in having an antihypertensive effect. Hypertension Research (2009) 32, 229-237; doi: 10.1038/hr.2009.5; published online 27 February 2009
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