Evidence map›Paper›PMID 28899893›Full record

ArticleJournal of the American Heart Association2017

Acute In Vivo Analysis of ATP Release in Rat Kidneys in Response to Changes of Renal Perfusion Pressure.

Oleg Palygin, Louise C Evans, Allen W Cowley, Alexander Staruschenko

Open access · goldAbstract read
In one paragraph

Article in Journal of the American Heart Association, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.6field-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

21 citing papers in PubMed, 26 citations in OpenAlex.

  1. GPER1 activation regulates renal purinergic P2YAmerican journal of physiology. Regulatory, integrative and comparative physiology · 2026
    Article
  2. Review
  3. Review
  4. Immunological insights into hypertension: unraveling triggers and potential therapeutic avenues.Hypertension research : official journal of the Japanese Society of Hypertension · 2024
    Review
  5. Calcium signalling and transport in the kidney.Nature reviews. Nephrology · 2024
    Review
  6. Review
  7. Hypertension (Dallas, Tex. : 1979) · 2024
    Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. NOX4-dependent regulation of ENaC in hypertension and diabetic kidney disease.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020
    Article
  13. Review
  14. Review
  15. Purinergic P2XAmerican journal of physiology. Renal physiology · 2020
    Article
  16. Review
  17. Review
  18. Article
  19. Article
  20. 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 1 institution in 1 country.

Oleg PalyginDepartment of Physiology, Medical College of Wisconsin, Milwaukee, WI.
Louise C EvansDepartment of Physiology, Medical College of Wisconsin, Milwaukee, WI.
Allen W CowleyDepartment of Physiology, Medical College of Wisconsin, Milwaukee, WI.
Alexander StaruschenkoDepartment of Physiology, Medical College of Wisconsin, Milwaukee, WI staruschenko@mcw.edu.
Medical College of Wisconsin · US

Funding

TRANSGENIC COREP60DK020595 · NIDDK · UNIVERSITY OF CHICAGO · PI BELL, GRAEME I · 1985 to 2012
$25.5M
Pilot and Feasibility ProgramP30DK020595 · NIDDK · UNIVERSITY OF CHICAGO · PI Raghavendra G Mirmira · 2013 to 2026
$20.9M
Renal ion channels in the control of blood pressureR35HL135749 · NHLBI · UNIVERSITY OF SOUTH FLORIDA · PI STARUSCHENKO, ALEXANDER · 2017 to 2023
$3.6M
Role of NOX4 In Kidney Function In Salt-Sensitive HypertensionR01HL122662 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI COWLEY, ALLEN W, STARUSCHENKO, ALEXANDER · 2015 to 2018
$1.5M
American Heart Association-American Stroke Association 16EIA26720006NHLBI NIH HHS R01 HL122662NHLBI NIH HHS R35 HL135749NIDDK NIH HHS P30 DK020595NIDDK NIH HHS P60 DK020595
6 · The paper itself

Abstract

backgroundATP and derivatives are recognized to be essential agents of paracrine signaling. It was reported that ATP is an important regulator of the pressure-natriuresis mechanism. Information on the sources of ATP, the mechanisms of its release, and its relationship to blood pressure has been limited by the inability to precisely measure dynamic changes in intrarenal ATP levels in vivo. METHODS AND

resultsNewly developed amperometric biosensors were used to assess alterations in cortical ATP concentrations in response to changes in renal perfusion pressure (RPP) in anesthetized Sprague-Dawley rats. RPP was monitored via the carotid artery; ligations around the celiac/superior mesenteric arteries and the distal aorta were used for manipulation of RPP. Biosensors were acutely implanted in the renal cortex for assessment of ATP. Rise of RPP activated diuresis/natriuresis processes, which were associated with elevated ATP. The increases in cortical ATP concentrations were in the physiological range (1-3 μmol/L) and would be capable of activating most of the purinergic receptors. There was a linear correlation with every 1-mm Hg rise in RPP resulting in a 70-nmol/L increase in ATP. Furthermore, this elevation of RPP was accompanied by a 2.5-fold increase in urinary H

conclusionsChanges in RPP directly correlate with renal sodium excretion and the elevation of cortical ATP. Given the known effects of ATP on regulation of glomerular filtration and tubular transport, the data support a role for ATP release in the rapid natriuretic responses to acute increases in RPP.

Indexed as

Blood PressureMechanotransduction, CellularParacrine CommunicationRenal CirculationAdenosine TriphosphateAnimalsBiosensing TechniquesHydrogen PeroxideKidneyMaleNatriuresisRats, Sprague-DawleyReceptors, Purinergic P2Time FactorsAdenosine TriphosphateHydrogen PeroxideReceptors, Purinergic P2ATPhypertensionkidneyP2 receptorspressure natriuresispurinergic signalingrenal

Identifiers

PMID28899893
PMCPMC5634305
OpenAlexW2754653296

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.