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Published on: December 21, 2011
Causal link between oxidative stress, inflammation, and hypertension
1Department of Medicine, University of California, Irvine, California, USA. ndvaziri@uci.edu
Insights
Hypertension (HTN) involves a harmful cycle of oxidative stress and inflammation, damaging organs. Interrupting this cycle is key to managing HTN and its complications.
Area of Science:
- Cardiovascular Medicine
- Pathophysiology
Background:
- Hypertension (HTN) is a significant risk factor for severe cardiovascular and renal diseases.
- Oxidative stress and inflammation are integral to the development and progression of HTN and its complications.
Purpose of the Study:
- To review the role of oxidative stress and inflammation in HTN pathogenesis.
- To examine HTN's contribution to oxidative stress and inflammation.
- To discuss the tissue angiotensin system's role and treatment strategies for HTN-associated oxidative stress.
Main Methods:
- Literature review of existing evidence.
- Analysis of the interplay between HTN, oxidative stress, and inflammation.
- Examination of the tissue angiotensin system's involvement.
Main Results:
- Evidence supports a self-perpetuating cycle involving HTN, oxidative stress, and inflammation.
- This cycle leads to progressive target organ damage.
- The tissue angiotensin system plays a role in this cycle.
Conclusions:
- Oxidative stress and inflammation are critical in HTN pathogenesis and complications.
- Targeting this cycle, including the tissue angiotensin system, is a potential therapeutic approach.
Abstract:
Hypertension (HTN) is a major cause of stroke, left ventricular hypertrophy, congestive heart failure, arteriosclerosis, end-stage renal disease, and peripheral vascular disease. Oxidative stress and its constant companion, inflammation, play a critical part in the pathogenesis of many acute and chronic illnesses including HTN and its long-term complications. There is compelling evidence that oxidative stress, inflammation, and HTN are involved in a self-perpetuating vicious cycle which, if not interrupted, culminates in progressive target organ injury and dysfunction. This article is intended to review the available evidence for the role of oxidative stress and inflammation in the pathogenesis of HTN. In addition, evidence will be presented to demonstrate the role of HTN in the pathogenesis of oxidative stress and inflammation. Finally, evidence for participation of tissue angiotensin system in the vicious cycle of oxidative stress, inflammation, and HTN will be presented, and the approach to treatment of HTN-associated oxidative stress will be discussed.
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