Evidence map›Paper›PMID 22490446›Full record

ArticlePeptides2012

Divergent pathways for the angiotensin-(1-12) metabolism in the rat circulation and kidney.

Brian M Westwood, Mark C Chappell

Abstract read
In one paragraph

Article in Peptides, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.7field-weighted citation impact, top 9% 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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

23 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
  2. Article
  3. An Update on the Tissue Renin Angiotensin System and Its Role in Physiology and Pathology.Journal of cardiovascular development and disease · 2019 · on this map
    Review
  4. Nicotine and the renin-angiotensin system.American journal of physiology. Regulatory, integrative and comparative physiology · 2018
    Review
  5. Article
  6. Article
  7. Measurement of Angiotensin Peptides: HPLC-RIA.Methods in molecular biology (Clifton, N.J.) · 2017
    Review
  8. Article
  9. Review
  10. Intracrine angiotensin II functions originate from noncanonical pathways in the human heart.American journal of physiology. Heart and circulatory physiology · 2016
    Review
  11. Biochemical evaluation of the renin-angiotensin system: the good, bad, and absolute?American journal of physiology. Heart and circulatory physiology · 2016
    Review
  12. Review
  13. Article
  14. Article
  15. Is the renin-angiotensin system actually hypertensive?Pediatric nephrology (Berlin, Germany) · 2014
    Review
  16. Article
  17. Review
  18. Review
  19. Review
  20. Primacy of angiotensin converting enzyme in angiotensin-(1-12) metabolism.American journal of physiology. Heart and circulatory physiology · 2013
    Article
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

2 authors at 1 institution in 1 country.

Brian M WestwoodThe Hypertension & Vascular Research Center, Wake Forest University Health Science Center, Winston-Salem, NC 27157, United States.
Mark C Chappell
Wake Forest University · US

Funding

Vaso-Hormonal Mechanisms in HypertensionP01HL051952 · NHLBI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI GROBAN, LEANNE · 1994 to 2019
$34.8M
Estrogen, ACE2 and Salt-SensitivityR01HL056973 · NHLBI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI CHAPPELL, MARK C · 2004 to 2008
$1.6M
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 HL056973
6 · The paper itself

Abstract

Evidence of endogenous angiotensin-(1-12) [Ang-(1-12)] may necessitate revision of the accepted view that Ang I is the immediate peptide product derived from the precursor protein angiotensinogen. As the processing of this peptide has not been fully elucidated, we characterized Ang-(1-12) metabolism in the serum and kidney of the mRen2.Lewis rat, a model of high circulating renin and ACE expression. A sensitive HPLC-based method to detect the metabolism ex vivo of low concentrations of (125)I-labeled Ang-(1-12) was utilized. Ang-(1-12) processing to serum did not reveal the participation of renin; however, serum ACE readily converted Ang-(1-12) to Ang I with subsequent metabolism to Ang II. Ang I and Ang II forming activities for serum ACE were 102±4 and 104±3 fmol/ml/min serum (n=3), respectively, and both products were abolished by the potent ACE inhibitor lisinopril. The metabolism of Ang-(1-12) in renal cortical membranes also revealed the formation of Ang I; however, the main products were Ang-(1-7) and Ang-(1-4) at 129±9 and 310±12 fmol/mg/min protein (n=4), respectively. Neprilysin inhibition abolished these products and substantially reduced the overall metabolism of Ang-(1-12). Incubation of Ang-(1-12) with either human or mouse neprilysin revealed identical products. We conclude that endogenous Ang-(1-12) may contribute to the expression of biologically active angiotensins through a renin-independent pathway. The preferred route for Ang-(1-12) metabolism likely reflects the relative tissue content of ACE and neprilysin.

Indexed as

Angiotensin-Converting Enzyme InhibitorsAngiotensin IAngiotensin IIAngiotensinogenAngiotensinsAnimalsHypertensionKidneyLisinoprilMaleNeprilysinPeptide FragmentsPeptidyl-Dipeptidase ARatsRats, Inbred LewReninAngiotensin-Converting Enzyme InhibitorsAngiotensin IAngiotensin IIAngiotensinogenAngiotensinsLisinoprilNeprilysinPeptide FragmentsPeptidyl-Dipeptidase Aproangiotensin-12, ratRenin

Identifiers

PMID22490446
PMCPMC3366343
OpenAlexW2122945293

What OpenQuestion holds

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Read underepoch 390

Registered trials

None linked

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.