Evidence map›Paper›PMID 12949225›Full record

ReviewThe Journal of physiology2003

Renin: origin, secretion and synthesis.

Pontus B Persson

Registry-linked trialOpen access · bronzeAbstract readReview
In one paragraph

Review in The Journal of physiology, 2003. 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 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
2.0field-weighted citation impact, top 12% 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.

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

47 citing papers in PubMed, 150 citations in OpenAlex.

  1. Trial
  2. Review
  3. Review
  4. Renal interoception in health and disease.Autonomic neuroscience : basic & clinical · 2024
    Review
  5. Review
  6. Validity of mental and physical stress models.Neuroscience and biobehavioral reviews · 2024
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Anticipated pharmacological role of Aviptadil on COVID-19.Environmental science and pollution research international · 2022
    Review
  15. Review
  16. Article
  17. Review
  18. Review
  19. Article
  20. 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

1 author at 1 institution in 1 country.

Pontus B PerssonJohannes-Müller-Institut für Physiologie, Humboldt Universität, Berlin (Medizinische Fakultät, Charité), Germany. pontus.persson@charite.de
Charité - Universitätsmedizin Berlin · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Renin is a central hormone in the control of blood pressure and various other physiological functions. In spite of the very early discovery of renin over 100 years ago, we have only recently gained a deeper understanding of the origin of renin-producing cells and of the mechanisms responsible for renin synthesis and secretion. The main source of renin is the juxtaglomerular cells (JGCs), which release renin from storage granules. Besides the renin-angiotensin system (RAS) in the JGCs, there exist local RASs in various tissues. JGCs originate in situ within the metanephric kidney from mesenchymal cells that are not related to smooth muscle lineages, as hitherto assumed. The previous notion that JGCs stem from vascular smooth muscle cells may be explained by JGC differentiation: they acquire smooth muscle markers that are maintained throughout adulthood. It has become clear that increasing intracellular free [Ca2+] inhibits renin secretion in JGCs. In contrast, cAMP stimulates renin release. Over the last decade, numerous studies on isolated JGCs and intact animals have provided contradictory results as to whether cGMP has a stimulatory or inhibitory action on renin release. More recent results strongly suggest that the effects of cGMP on renin release from JGCs involve the degradation of cAMP, which is modulated by cGMP. Finally, it has been found that not only is the production of renin modulated by enhancing or attenuating renin transcription, but renin mRNA stability is controlled by various proteins present in renin-producing cells.

Indexed as

AnimalsCyclic AMPCyclic GMPHumansJuxtaglomerular ApparatusReninCyclic AMPCyclic GMPRenin

Identifiers

PMID12949225
PMCPMC2343457
OpenAlexW2046571833

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.