Evidence map›Paper›PMID 26475588›Full record

ReviewAmerican journal of physiology. Heart and circulatory physiology2016

Biochemical evaluation of the renin-angiotensin system: the good, bad, and absolute?

Mark C Chappell

Registry-linked trialAbstract readReview
In one paragraph

Review in American journal of physiology. Heart and circulatory physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04752293 (Pediatric Hypertension and the Renin-Angiotensin SystEm), which is not on this map. Cited by 171 papers.

0numbers the graph read from it
0cells of the map it votes in
171citing papers in PubMed
12.5field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

NCT04752293 recruitingnot on this mapstarted 2021, after this paper: background citation

Pediatric Hypertension and the Renin-Angiotensin SystEm (PHRASE): The Role of Angiotensin-(1-7) in Hypertension and Hypertension-Induced Heart and Kidney Damage

TypeobservationalSponsorWake Forest University Health SciencesRan2021 to 2026Enrolled125ConditionsHypertension, Left Ventricular Hypertrophy, Left Ventricular Dysfunction, Left Atrial Dilatation
3 · Its place in the literature

Who cites it

171 citing papers in PubMed, 284 citations in OpenAlex.

  1. Trial
  2. Trial
  3. A pilot study to assess the circulating renin-angiotensin system in COVID-19 acute respiratory failure.American journal of physiology. Lung cellular and molecular physiology · 2021
    Trial
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Angiotensin Dysregulation in Patients with Arterial Aneurysms.International journal of molecular sciences · 2025
    Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Review

111 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

Mark C ChappellThe Hypertension and Vascular Research Center, Wake Forest University School of Medicine, Winston-Salem, North Carolina mchappel@wakehealth.edu.
Wake Forest University · US

Funding

Vaso-Hormonal Mechanisms in HypertensionP01HL051952 · NHLBI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI DELL'ITALIA, LOUIS J. · 1994 to 2019
$34.8M
The Impact of Antenatal Steroid Exposure on the Intrarenal Renin-Angiotensin SystP01HD047584 · NICHD · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI ROSE, JAMES C. · 2005 to 2016
$13.0M
FETAL ENDOCRINE-CARDIOVASCULAR RELATIONSHIPSR01HD017644 · NICHD · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI ROSE, JAMES C. · 1985 to 2011
$2.8M
Estrogen, ACE2 and Salt-SensitivityR01HL056973 · NHLBI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI CHAPPELL, MARK C · 2004 to 2008
$1.6M
Novel Angiotensin-(1-7) Endopeptidase in Fetal ProgrammingR21HD084227 · NICHD · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI CHAPPELL, MARK C, ROSE, JAMES C. · 2016 to 2017
$426k
REGULATION AND FUNCTION OF ANGIOTENSIN (1-7)R29HL056973 · NHLBI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI CHAPPELL, MARK C · 1996 to 1999
–
NHLBI NIH HHS HL-51952NHLBI NIH HHS HL-56973NHLBI NIH HHS P01 HL051952NHLBI NIH HHS R01 HL056973NHLBI NIH HHS R29 HL056973NICHD NIH HHS HD-047584NICHD NIH HHS HD-084227NICHD NIH HHS P01 HD047584NICHD NIH HHS R01 HD017644NICHD NIH HHS R21 HD084227
6 · The paper itself

Abstract

The renin-angiotensin system (RAS) constitutes a key hormonal system in the physiological regulation of blood pressure through peripheral and central mechanisms. Indeed, dysregulation of the RAS is considered a major factor in the development of cardiovascular pathologies, and pharmacological blockade of this system by the inhibition of angiotensin-converting enzyme (ACE) or antagonism of the angiotensin type 1 receptor (AT1R) offers an effective therapeutic regimen. The RAS is now defined as a system composed of different angiotensin peptides with diverse biological actions mediated by distinct receptor subtypes. The classic RAS comprises the ACE-ANG II-AT1R axis that promotes vasoconstriction; water intake; sodium retention; and increased oxidative stress, fibrosis, cellular growth, and inflammation. In contrast, the nonclassical RAS composed primarily of the ANG II/ANG III-AT2R and the ACE2-ANG-(1-7)-AT7R pathways generally opposes the actions of a stimulated ANG II-AT1R axis. In lieu of the complex and multifunctional aspects of this system, as well as increased concerns on the reproducibility among laboratories, a critical assessment is provided on the current biochemical approaches to characterize and define the various components that ultimately reflect the status of the RAS.

Indexed as

AnimalsBiomarkersBlood PressureHeart DiseasesHumansRenin-Angiotensin SystemBiomarkersACEangiotensinheartrenin

Identifiers

PMID26475588
PMCPMC4796631
OpenAlexW2279350596

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.