Evidence map›Paper›PMID 26370892›Full record

ArticleHypertension (Dallas, Tex. : 1979)2015

Role of the Paraventricular Nucleus of the Hypothalamus in the Sympathoexcitatory Effects of Leptin.

Zhigang Shi, Baoxin Li, Virginia L Brooks

Open access · bronzeAbstract read
In one paragraph

Article in Hypertension (Dallas, Tex. : 1979), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

41 citing papers in PubMed, 57 citations in OpenAlex.

  1. Article
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  4. Review
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  9. Article
  10. Article
  11. Review
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  13. Article
  14. Glomerular hyperfiltration.Nature reviews. Nephrology · 2022
    Review
  15. Article
  16. Article
  17. Review
  18. Obesity, Hypertension, and Bariatric Surgery.Current hypertension reports · 2020
    Review
  19. Article
  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

3 authors at 1 institution in 1 country.

Zhigang ShiFrom the Department of Physiology and Pharmacology, Oregon Health & Science University, Portland, OR.
Baoxin LiFrom the Department of Physiology and Pharmacology, Oregon Health & Science University, Portland, OR.
Virginia L BrooksFrom the Department of Physiology and Pharmacology, Oregon Health & Science University, Portland, OR. brooksv@ohsu.edu.
Oregon Health & Science University · US

Funding

Oregon Clinical and Translational Research InstituteUL1TR000128 · NCATS · OREGON HEALTH & SCIENCE UNIVERSITY · PI ELLISON, DAVID H · 2012 to 2015
$28.7M
Insulin Resistance and Impaired Cardiovascular Regulation During PregnancyR01HL088552 · NHLBI · OREGON HEALTH & SCIENCE UNIVERSITY · PI BROOKS, VIRGINIA L. · 2008 to 2011
$1.6M
NCATS NIH HHS UL1 TR000128NCATS NIH HHS UL1TR000128NHLBI NIH HHS HL088552NHLBI NIH HHS R01 HL088552
6 · The paper itself

Abstract

Leptin binds to receptors in multiple hypothalamic nuclei to increase sympathetic nerve activity; however, the neurocircuitry is unclear. Here, using anesthetized male Sprague-Dawley rats, we investigated the role of the paraventricular nucleus of the hypothalamus. Intracerebroventricular injection of leptin slowly increased lumbar sympathetic nerve activity (LSNA), heart rate, mean arterial pressure, and baroreflex control of LSNA and heart rate. Inhibition of the paraventricular nucleus with muscimol completely reversed leptin's effects. Blockade of paraventricular melanocortin 3/4 receptors with SHU9119 or ionotropic glutamate receptors with kynurenate, alone or together, each partially reversed the effects of leptin, implicating increased activation of glutamate and melanocortin 3/4 receptors. Conversely, although blockade of neuropeptide Y Y1 receptors in the paraventricular nucleus increased LSNA, mean arterial pressure, and heart rate, these responses were prevented by intracerebroventricular or arcuate nucleus injections of leptin, suggesting that, at least in part, leptin also increases sympathetic nerve activity by suppression of tonic neuropeptide Y inhibitory inputs from the arcuate nucleus. Injection of the melanocortin 3/4 receptor agonist melanotan-II into the paraventricular nucleus increased LSNA, mean arterial pressure, and heart rate only after blockade of neuropeptide Y Y1 receptors. Therefore, we conclude that leptin increases LSNA in part via increased glutamatergic and α-melanocyte-stimulating hormone drive of paraventricular sympathoexcitatory neurons, the latter of which requires simultaneous withdrawal of tonic neuropeptide Y inhibition.

Indexed as

alpha-MSHAnimalsBlood PressureGlutamic AcidHeart RateHypothalamusLeptinMaleModels, AnimalNeuropeptide YParaventricular Hypothalamic NucleusRatsRats, Sprague-DawleySympathetic Nervous Systemalpha-MSHGlutamic AcidLeptinNeuropeptide Yarcuate nucleusarterial pressurebaroreflexBIBO 3304kynurenateSHU9119

Identifiers

PMID26370892
PMCPMC4798233
OpenAlexW2175939167

What OpenQuestion holds

Textmetadata
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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.