Evidence map›Paper›PMID 24303192›Full record

ArticlePhysiological reports2013

OVLT lesion decreases basal arterial pressure and the chronic hypertensive response to AngII in rats on a high-salt diet.

John P Collister, Marin K Olson, David B Nahey, Alexandre A Vieira, John W Osborn

Open access · goldAbstract read
In one paragraph

Article in Physiological reports, 2013. 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
2.2field-weighted citation impact, top 11% 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, 26 citations in OpenAlex.

  1. The organum vasculosum of the lamina terminalis contributes to neurohumoral mechanisms of renal vascular hypertension.American journal of physiology. Regulatory, integrative and comparative physiology · 2025
    Article
  2. Article
  3. Review
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  7. DOCA-salt hypertension and the role of the OVLT-sympathetic-gut microbiome axis.Clinical and experimental pharmacology & physiology · 2021
    Article
  8. Review
  9. Lesion of the OVLT markedly attenuates chronic DOCA-salt hypertension in rats.American journal of physiology. Regulatory, integrative and comparative physiology · 2018
    Article
  10. Article
  11. Article
  12. Review
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  14. Possible role for brain prostanoid pathways in the development of angiotensin II-salt hypertension in rats.American journal of physiology. Regulatory, integrative and comparative physiology · 2016
    Article
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  16. Review
  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

5 authors at 1 institution in 1 country.

John P CollisterDepartment of Veterinary and Biomedical Sciences, College of Veterinary Medicine, University of Minnesota St. Paul, MN.
Marin K Olson
David B Nahey
Alexandre A Vieira
John W Osborn
University of Minnesota · US

Funding

Targeted Sympathetic Ablation for Treatment of HypertensionR01HL116476 · NHLBI · UNIVERSITY OF MINNESOTA · PI OSBORN, JOHN W · 2014 to 2022
$3.9M
NHLBI NIH HHS R01 HL116476
6 · The paper itself

Abstract

We have reported that lesion of the organum vasculosum of the lamina terminalis (OVLT) has no effect on basal levels of mean arterial pressure (MAP) but abolishes the hypertensive effects of angiotensin II (AngII) in rats consuming a normal-salt diet. These results suggest that the OVLT does not contribute to regulation of MAP under conditions of normal salt intake, but it is an important brain site for the hypertensive actions of AngII. The OVLT has been proposed as a major sodium sensor in the brain and the hypertensive effects of AngII are exacerbated by high-salt intake. Therefore, the objective of this study was to investigate the role of the OVLT during AngII-induced hypertension in rats fed a high-salt diet. Male Sprague-Dawley rats underwent sham (Sham; n = 9) or OVLT lesion (OVLTx; n = 8) surgery and were placed on a high-salt (2% NaCl) diet. MAP was measured by radio telemetry during three control days, 10 days of AngII infusion (10 ng/kg/min, i.v.), and a 3-day recovery period. MAP was significantly lower in OVLTx (97 ± 2 mmHg) compared to Sham (106 ± 1 mmHg) rats during the control period (P < 0.05). Moreover, the chronic pressor response to AngII was markedly attenuated in OVLTx rats. MAP increased 58 ± 3 mmHg in Sham rats by Day 10 of AngII compared to a 40 ± 7 mmHg increase in OVLTx rats (P < 0.05). We conclude that (1) the OVLT regulates the basal levels of MAP in rats consuming a high-salt and (2) the OVLT is an important brain site of action for the pathogenesis of AngII-salt hypertension in the rat. Supported by HL076312.

Indexed as

Angtiotensin IIcircumventricular organhypertensionOVLT

Identifiers

PMID24303192
PMCPMC3841056
OpenAlexW2132653220

What OpenQuestion holds

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LicenceCC BY
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.