Evidence map›Paper›PMID 23720263›Full record

ReviewComprehensive Physiology2012

Nonclassical renin-angiotensin system and renal function.

Mark C Chappell

Registry-linked trialAbstract readReview
In one paragraph

Review in Comprehensive Physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06539234 (Angiotensin II Stress Test. Renin Kinetics During Treatment of Vasoplegic Shock With Angiotensin II in Relation to Hemodynamic Response to Treatment With Angiotensin II.), which is not on this map. Cited by 77 papers.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed
–field-weighted citation impact
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.

NCT06539234 recruitingnot on this mapstarted 2024, after this paper: background citation

Angiotensin II Stress Test. Renin Kinetics During Treatment of Vasoplegic Shock With Angiotensin II in Relation to Hemodynamic Response to Treatment With Angiotensin II.

TypeobservationalSponsorUniversity Medical Centre MariborRan2024 to 2026Enrolled80ConditionsShock, Vasoplegic Syndrome
3 · Its place in the literature

Who cites it

77 citing papers in PubMed, 130 citations in OpenAlex.

  1. Article
  2. The relationship between estrogen and renin angiotensin system components in the context of hypertension.Hypertension research : official journal of the Japanese Society of Hypertension · 2025
    Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Angiotensin II-Real-Life Use and Literature Review.Medicina (Kaunas, Lithuania) · 2024
    Review
  9. Renin-angiotensin system-mediated nitric oxide signaling in podocytes.American journal of physiology. Renal physiology · 2024
    Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Review
  16. Review
  17. Review
  18. Challenges of COPD Patients during the COVID-19 Pandemic.Pathogens (Basel, Switzerland) · 2022
    Review
  19. Review
  20. Angiotensin II enhances bacterial clearance via myeloid signaling in a murine sepsis model.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article

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

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

Mark C ChappellThe Hypertension & Vascular Disease Center, Department of Physiology & Pharmacology, Wake Forest University School of Medicine, Winston-Salem, North Carolina, USA. mchappel@wakehealth.edu
Wake Forest University · US

Funding

Vaso-Hormonal Mechanisms in HypertensionP01HL051952 · NHLBI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI GROBAN, LEANNE · 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
Establishment of a model for diabetic cardiorenal syndrome in female mRen2.LewisR21HL112237 · NHLBI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI CHAPPELL, MARK C, VARAGIC, JASMINA · 2012 to 2013
$398k
REGULATION AND FUNCTION OF ANGIOTENSIN (1-7)R29HL056973 · NHLBI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI CHAPPELL, MARK C · 1996 to 1999
–
NHLBI NIH HHS HL112237NHLBI NIH HHS HL-51952NHLBI NIH HHS HL-56973NHLBI NIH HHS P01 HL051952NHLBI NIH HHS R01 HL056973NHLBI NIH HHS R21 HL112237NHLBI NIH HHS R29 HL056973NICHD NIH HHS HD017644NICHD NIH HHS HD047584NICHD NIH HHS P01 HD047584NICHD NIH HHS R01 HD017644
6 · The paper itself

Abstract

The renin-angiotensin system (RAS) constitutes one of the most important hormonal systems in the physiological regulation of blood pressure through renal and nonrenal mechanisms. Indeed, dysregulation of the RAS is considered a major factor in the development of cardiovascular pathologies, including kidney injury, and blockade of this system by the inhibition of angiotensin converting enzyme (ACE) or blockade of the angiotensin type 1 receptor (AT1R) by selective antagonists constitutes an effective therapeutic regimen. It is now apparent with the identification of multiple components of the RAS within the kidney and other tissues that the system is actually composed of different angiotensin peptides with diverse biological actions mediated by distinct receptor subtypes. The classic RAS can be defined as the ACE-Ang II-AT1R axis that promotes vasoconstriction, water intake, sodium retention, and other mechanisms to maintain blood pressure, as well as increase oxidative stress, fibrosis, cellular growth, and inflammation in pathological conditions. In contrast, the nonclassical RAS composed primarily of the AngII/Ang III-AT2R pathway and the ACE2-Ang-(1-7)-AT7R axis generally opposes the actions of a stimulated Ang II-AT1R axis through an increase in nitric oxide and prostaglandins and mediates vasodilation, natriuresis, diuresis, and reduced oxidative stress. Moreover, increasing evidence suggests that these non-classical RAS components contribute to the therapeutic blockade of the classical system to reduce blood pressure and attenuate various indices of renal injury, as well as contribute to normal renal function.

Indexed as

AminopeptidasesAngiotensinsBlood PressureEndopeptidasesHumansKidneyPeptidyl-Dipeptidase AReninRenin-Angiotensin SystemSignal TransductionAminopeptidasesAngiotensinsEndopeptidasesPeptidyl-Dipeptidase ARenin

Identifiers

PMID23720263
PMCPMC4186703
OpenAlexW1567635264

What OpenQuestion holds

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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.