ArticleFrontiers in physiology2016
Modeling Disease Progression: Angiotensin II Indirectly Inhibits Nitric Oxide Production via ADMA Accumulation in Spontaneously Hypertensive Rats.
Article in Frontiers in physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 9 citations in OpenAlex.
- Angiotensin Regulation of Vascular Homeostasis: Exploring the Role of ROS and RAS Blockers.International journal of molecular sciences · 2023Review
- A novel role of kallikrein-related peptidase 8 in the pathogenesis of diabetic cardiac fibrosis.Theranostics · 2021Article
- Impaired Endothelial Function in Hereditary Angioedema During the Symptom-Free Period.Frontiers in physiology · 2018Article
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7 authors at 1 institution in 1 country.
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Abstract
Nitric oxide (NO) production impairment is involved in the onset and development of hypertension. Although NO production impairment in spontaneously hypertensive rat (SHR) has been reported in a variety of researches, the time course of this progressive procedure, as well as its relationship with asymmetric dimethylarginine (ADMA) and angiotensin II (Ang II), has not been quantified. The aim of this research is to establish a mechanism-based disease progression model to assess Ang II and ADMA's inhibition of NO production in SHR's disease progression with/without ramipril's intervention. SHR were randomly divided into three groups: one disease group (
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