Evidence map›Paper›PMID 21971830›Full record

ReviewCurrent hypertension reports2011

Effects of relaxin on arterial dilation, remodeling, and mechanical properties.

Kirk P Conrad, Sanjeev G Shroff

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current hypertension reports, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 1 pooled it
5.7field-weighted citation impact, top 5% 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

42 citing papers in PubMed, 1 synthesis or guideline pooled it, 87 citations in OpenAlex.

  1. Pooled it
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  5. Review
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  14. Article
  15. The actions of relaxin on the human cardiovascular system.British journal of pharmacology · 2017
    Review
  16. Anti-fibrotic actions of relaxin.British journal of pharmacology · 2017
    Review
  17. Review
  18. Vascular actions of relaxin: nitric oxide and beyond.British journal of pharmacology · 2017
    Review
  19. Review
  20. Review
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 2 institutions in 2 countries.

Kirk P ConradDepartment of Physiology and Functional Genomics, D.H. Barron Reproductive and Perinatal Biology Research Program, University of Florida, 1600 SW Archer Road, Gainesville, FL 32610, USA. kpconrad@ufl.edu
Sanjeev G Shroff
Florida College · USUniversity of Pittsburgh · US

Funding

Relaxin: The 'Elusive'Vasodilator of PregnancyR01HL067937 · NHLBI · UNIVERSITY OF FLORIDA · PI CONRAD, KIRK P · 2001 to 2009
$2.2M
Mechanisms of Vasodilation in PregancyR01DK063321 · NIDDK · UNIVERSITY OF FLORIDA · PI CONRAD, KIRK P · 2002 to 2005
$1.1M
NITRIC OXIDE AND MATERNAL HEMODYNAMICS IN PREGNANCYR01HD030325 · NICHD · UNIVERSITY OF NEW MEXICO · PI CONRA, KIRK P · 1994 to 2001
$473k
GLOMERULAR FUNCTION/BLOOD PRESSURE--PREGNANCYK11HD000662 · NICHD · DARTMOUTH COLLEGE · PI CONRA, KIRK P · 1985 to 1989
–
NHLBI NIH HHS R01 HL067937NHLBI NIH HHS R21 HL093334NICHD NIH HHS (K11 HD00662NICHD NIH HHS R01 HD030325NIDDK NIH HHS R01 DK063321
6 · The paper itself

Abstract

Administering relaxin to conscious rats and humans elicits systemic and renal vasodilation. The molecular mechanisms vary according to the duration of relaxin exposure-so-called "rapid" (within minutes) or "sustained" (hours to days) vasodilatory responses-both being endothelium-dependent. Rapid responses are mediated by G(αi/o) protein coupling to phosphoinositol-3 kinase/Akt (protein kinase B)-dependent phosphorylation and activation of nitric oxide synthase. Sustained responses are mediated by vascular endothelial and placental growth factors, as well as increases in arterial gelatinase activity. Thus, after hours or days of relaxin treatment, respectively, arterial MMP-9 or MMP-2 hydrolyze "big" endothelin (ET) at a gly-leu bond to form ET(1-32), which in turn activates the endothelial ET(B) receptor/nitric oxide vasodilatory pathway. Administration of relaxin to conscious rats also increases global systemic arterial compliance and passive compliance of select isolated blood vessels such as small renal arteries (SRA). The increase in SRA passive compliance is mediated by both geometric remodeling (outward) and compositional remodeling (decreased collagen). Relaxin-induced geometric remodeling has also been observed in brain parenchymal arteries, and this remodeling appears to be via the activation of peroxisome proliferator-activated receptor-γ. Given the vasodilatory and arterial remodeling properties of relaxin, the hormone may have therapeutic potential in the settings of abnormal pregnancies, heart failure, and pathologies associated with stiffening of arteries.

Indexed as

AnimalsArteriesBiomechanical PhenomenaDisease Models, AnimalEndothelium, VascularFemaleHeart FailureHumansHypertensionPre-EclampsiaPregnancyRelaxinReproductive Techniques, AssistedVasodilationRelaxin

Identifiers

PMID21971830
OpenAlexW2012271024

What Socratic 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 Socratic graph.