Evidence map›Paper›PMID 22565307›Full record

ArticleThe Journal of clinical investigation2012

Genetic modifiers of hypertension in soluble guanylate cyclase α1-deficient mice.

Emmanuel S Buys, Michael J Raher, Andrew Kirby, Mohd Shahid, Shahid Mohd, David M Baron, Sarah R Hayton, Laurel T Tainsh, Patrick Y Sips, Kristen M Rauwerdink and 12 more

Erratum issuedAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing 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.

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

20 citing papers in PubMed.

  1. Trial
  2. Article
  3. Article
  4. Age Impairs Soluble Guanylyl Cyclase Function in Mouse Mesenteric Arteries.International journal of molecular sciences · 2021
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Genetic modification of hypertension by sGCα1.Trends in cardiovascular medicine · 2013
    Review
  17. Assessing murine resistance artery function using pressure myography.Journal of visualized experiments : JoVE · 2013
    Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

  • Erratum issued
    Mohd, Shahid [corrected to Shahid, Mohd]
5 · Who and what money

Authors and funding

22 authors.

Emmanuel S BuysAnesthesia Center for Critical Care Research, Department of Anesthesia, Critical Care, and Pain Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts 02114, USA. Ebuys@partners.org
Michael J Raher
Andrew Kirby
Mohd Shahid
Shahid Mohd
David M Baron
Sarah R Hayton
Laurel T Tainsh
Patrick Y Sips
Kristen M Rauwerdink
Qingshang Yan
Robert E T Tainsh
Hannah R Shakartzi
Christine Stevens
Kelly Decaluwé
Maria da Gloria Rodrigues-Machado
Rajeev Malhotra
Johan Van de Voorde
Tong Wang
Peter Brouckaert
Mark J Daly
Kenneth D Bloch

Funding

Renal Physiology and Phenotyping CoreP30DK079310 · NIDDK · YALE UNIVERSITY · PI ARONSON, PETER S. · 2008 to 2022
$16.8M
BMPR2 and the Pathogenesis of Pulmonary HypertensionR01HL074352 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI BLOCH, KENNETH D · 2003 to 2011
$3.7M
NHLBI NIH HHS R01 HL074352NHLBI NIH HHS R01 HL74352NIDDK NIH HHS P30 DK079310
6 · The paper itself

Abstract

Nitric oxide (NO) plays an essential role in regulating hypertension and blood flow by inducing relaxation of vascular smooth muscle. Male mice deficient in a NO receptor component, the α1 subunit of soluble guanylate cyclase (sGCα1), are prone to hypertension in some, but not all, mouse strains, suggesting that additional genetic factors contribute to the onset of hypertension. Using linkage analyses, we discovered a quantitative trait locus (QTL) on chromosome 1 that was linked to mean arterial pressure (MAP) in the context of sGCα1 deficiency. This region is syntenic with previously identified blood pressure-related QTLs in the human and rat genome and contains the genes coding for renin. Hypertension was associated with increased activity of the renin-angiotensin-aldosterone system (RAAS). Further, we found that RAAS inhibition normalized MAP and improved endothelium-dependent vasorelaxation in sGCα1-deficient mice. These data identify the RAAS as a blood pressure-modifying mechanism in a setting of impaired NO/cGMP signaling.

Indexed as

Genome, HumanQuantitative Trait LociAnimalsCyclic GMPEndothelium, VascularFemaleGenetic LinkageGuanylate CyclaseHumansHypertensionMaleMiceMice, KnockoutRatsReceptors, Cytoplasmic and NuclearReninCyclic GMPGuanylate CyclaseReceptors, Cytoplasmic and NuclearReninSoluble Guanylyl Cyclase

Identifiers

PMID22565307
PMCPMC3366402

What OpenQuestion holds

Textmetadata
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.