Evidence map›Paper›PMID 21199648›Full record

ReviewEuropean journal of pharmacology2011

Cardiovascular effects of melanocortins.

Michael H Humphreys, Xi-Ping Ni, David Pearce

Abstract readReview
In one paragraph

Review in European journal of pharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.1field-weighted citation impact, top 28% 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

17 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Role of the brain melanocortins in blood pressure regulation.Biochimica et biophysica acta. Molecular basis of disease · 2017
    Review
  10. Article
  11. Article
  12. Approach to assessing determinants of glucose homeostasis in the conscious mouse.Mammalian genome : official journal of the International Mammalian Genome Society · 2014
    Review
  13. Review
  14. Review
  15. Article
  16. Article
  17. 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

3 authors at 2 institutions in 1 country.

Michael H HumphreysDivision of Nephrology, San Francisco General Hospital and Department of Medicine, University of California San Francisco, San Francisco, CA 94143, USA. mhumphreys@medsfgh.ucsf.edu
Xi-Ping Ni
David Pearce
San Francisco General Hospital · USUniversity of California, San Francisco · US

Funding

gamma-MSH and Sodium MetabolismR01HL068871 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI HUMPHREYS, MICHAEL H · 2003 to 2007
$1.7M
NHLBI NIH HHS HL68871NHLBI NIH HHS R01 HL068871
6 · The paper itself

Abstract

Melanocortins (MSH's) are three structurally related peptides derived from proopiomelanocortin. They regulate several physiologic functions including energy metabolism, appetite, and inflammation. Recent work in rodents has also identified important effects of MSH's, particularly γ-MSH, on sodium metabolism and blood pressure regulation. Normal rats and mice respond to a high sodium diet with an increase in the plasma concentration of γ-MSH, and remain normotensive, while those with genetic or pharmacologic γ-MSH deficiency become hypertensive on a high sodium diet. This hypertension is corrected by exogenous administration of the peptide. Mice lacking the γ-MSH receptor (the melanocortin 3 receptor, Mc3r) also become hypertensive on a high sodium diet but remain so when administered γ-MSH, and infusions of physiologic levels of the peptide stimulate urinary sodium excretion in normal rats and mice, but not in mice with deletion of Mc3r. The salt-sensitive hypertension in rodents with impaired γ-MSH signaling appears due to stimulation of noradrenergic activity, since plasma noradrenaline is increased and the hypertension is rapidly corrected with infusion of the α-adrenoceptor antagonist phentolamine. In contrast to the antihypertensive property of physiologic levels of γ-MSH, intravenous or intracerebroventricular injections of high levels of the peptide raise blood pressure. This occurs in mice lacking Mc3r, indicating an interaction with some other central receptor. Finally, the salt-sensitive hypertension in rodents with disruption of γ-MSH signaling is accompanied by insulin resistance, an observation which offers a new window into the study of the association of salt-sensitive hypertension with insulin resistance and type II diabetes.

Indexed as

AnimalsBlood PressureCardiovascular Systemgamma-MSHGlucoseHumansMelanocortinsSignal Transductiongamma-MSHGlucoseMelanocortins

Identifiers

PMID21199648
PMCPMC3086937
OpenAlexW2090422970

What OpenQuestion holds

Textmetadata
LicenceTDM
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.