Evidence map›Paper›PMID 28143710›Full record

ArticleAutonomic neuroscience : basic & clinical2017

Hepatic and renal mechanisms underlying the osmopressor response.

Tu H Mai, Emily M Garland, André Diedrich, David Robertson

Open access · greenAbstract read
In one paragraph

Article in Autonomic neuroscience : basic & clinical, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.2field-weighted citation impact, top 53% 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

2 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Independent endothelial functions of PIEZO1 and TRPV4 in hepatic portal vein and predominance of PIEZO1 in mechanical and osmotic stress.Liver international : official journal of the International Association for the Study of the Liver · 2023
    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

4 authors at 2 institutions in 1 country.

Tu H MaiDepartment of Pharmacology, Vanderbilt University, Nashville, TN, United States; Department of Clinical Pharmacology, Vanderbilt University, Nashville, TN, United States.
Emily M GarlandDepartment of Medicine, Vanderbilt University Medical Center, United States; Department of Clinical Pharmacology, Vanderbilt University, Nashville, TN, United States.
André DiedrichDepartment of Medicine, Vanderbilt University Medical Center, United States; Department of Biomedical Engineering, Vanderbilt University, United States; Department of Clinical Pharmacology, Vanderbilt University, Nashville, TN, United States.
David RobertsonDepartment of Pharmacology, Vanderbilt University, Nashville, TN, United States; Department of Medicine, Vanderbilt University Medical Center, United States; Department of Neurology, Vanderbilt University Medical Center, Nashville, TN, United States; Department of Clinical Pharmacology, Vanderbilt University, Nashville, TN, United States. Electronic address: david.robertson@vanderbilt.edu.
Vanderbilt University · USVanderbilt University Medical Center · US

Funding

Structural genomics of norepinephrine transportersP01HL056693 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI ROBERTSON, DAVID HERLIE · 1997 to 2016
$30.8M
NHLBI NIH HHS P01 HL056693
6 · The paper itself

Abstract

Increased blood pressure (BP) is observed in patients with impaired baroreflexes after water drinking. The stimulus for this effect is low blood osmolality, and it has been termed the osmopressor response (OPR). The BP increase is associated with activation of the sympathetic nervous system and a requirement for transient receptor potential vanilloid 4 (TRPV4) channels. However, the mechanisms underlying the OPR are poorly understood. We tested the hypothesis that hypotonicity is sensed in the portal area to initiate the OPR. Sino-aortic denervated mice were used and BP was monitored for 30min after fluid infusion while mice were under anesthesia. Infusion of hypotonic fluid (0.45% saline), but not of isotonic 0.9% saline, directly into the portal vein, produced an immediate OPR (increase in BP with saline 0.45%: 15±13 vs. 0.9%: -7±2mmHg, p=0.003; AUC: 0.45%: 150±99, n=7 vs. 0.9%: -74±60mmHg·min, n=5, p=0.003). However, 0.45% saline was not able to trigger a similar response in TRPV4

Indexed as

AnimalsAutonomic DenervationBaroreflexBlood PressureDrinkingDrinking WaterDuodenumHypotonic SolutionsJugular VeinsKidneyLiverMaleMice, Inbred C57BLMice, KnockoutModels, AnimalOsmolar ConcentrationDrinking WaterHypotonic SolutionsSodium Chloride, DietaryTrpv4 protein, mouseTRPV Cation ChannelsOsmopressor responsePortal infusionRenal denervationSino-aortic denervation

Identifiers

PMID28143710
PMCPMC5530865
OpenAlexW2581494800

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.