Evidence map›Paper›PMID 10097148›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1999

Blood pressure reduction and diabetes insipidus in transgenic rats deficient in brain angiotensinogen.

M Schinke, O Baltatu, M Böhm, J Peters, W Rascher, G Bricca, A Lippoldt, D Ganten, M Bader

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
5.6field-weighted citation impact, top 4% 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

55 citing papers in PubMed, 163 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. How Is the Brain Renin-Angiotensin System Regulated?Hypertension (Dallas, Tex. : 1979) · 2017
    Review
  10. No Brain Renin-Angiotensin System: Déjà vu All Over Again?Hypertension (Dallas, Tex. : 1979) · 2017
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Na+/Ca2+ exchange and Na+/K+-ATPase in the heart.The Journal of physiology · 2015
    Review
  16. Review
  17. Hypertension in mice with transgenic activation of the brain renin-angiotensin system is vasopressin dependent.American journal of physiology. Regulatory, integrative and comparative physiology · 2013
    Article
  18. Article
  19. Brain renin-angiotensin system in the nexus of hypertension and aging.Hypertension research : official journal of the Japanese Society of Hypertension · 2013
    Review
  20. The Angiotensin-melatonin axis.International journal of hypertension · 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

9 authors at 1 institution in 1 country.

M SchinkeMax-Delbrück-Center for Molecular Medicine (MDC), Robert-Rössle-Strasse 10, D-13092 Berlin-Buch, Germany.
O Baltatu
M Böhm
J Peters
W Rascher
G Bricca
A Lippoldt
D Ganten
M Bader
Max Delbrück Center · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Angiotensin produced systemically or locally in tissues such as the brain plays an important role in the regulation of blood pressure and in the development of hypertension. We have established transgenic rats [TGR(ASrAOGEN)] expressing an antisense RNA against angiotensinogen mRNA specifically in the brain. In these animals, the brain angiotensinogen level is reduced by more than 90% and the drinking response to intracerebroventricular renin infusions is decreased markedly compared with control rats. Blood pressure of transgenic rats is lowered by 8 mmHg (1 mmHg = 133 Pa) compared with control rats. Crossbreeding of TGR(ASrAOGEN) with a hypertensive transgenic rat strain exhibiting elevated angiotensin II levels in tissues results in a marked attenuation of the hypertensive phenotype. Moreover, TGR(ASrAOGEN) exhibit a diabetes insipidus-like syndrome producing an increased amount of urine with decreased osmolarity. The observed reduction in plasma vasopressin by 35% may mediate these phenotypes of TGR(ASrAOGEN). This new animal model presenting long-term and tissue-specific down-regulation of angiotensinogen corroborates the functional significance of local angiotensin production in the brain for the central regulation of blood pressure and for the pathogenesis of hypertension.

Indexed as

Angiotensin IIAngiotensinogenAnimalsAnimals, Genetically ModifiedArginine VasopressinBlood PressureBrainCerebral VentriclesDiabetes InsipidusElectrolytesExonsHypertensionHypotensionInjections, IntraventricularOrgan SpecificityRatsAngiotensin IIAngiotensinogenArginine VasopressinElectrolytesReninRNA, AntisenseRNA, Messenger

Identifiers

PMID10097148
PMCPMC22405
OpenAlexW1974133475

What OpenQuestion holds

Texttitle and abstract
measurements read3
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.