Evidence map›Paper›PMID 20519378›Full record

ArticleAmerican journal of physiology. Renal physiology2010

Adenosine A(2) receptors modulate tubuloglomerular feedback.

Mattias Carlström, Christopher S Wilcox, William J Welch

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Renal physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
3.6field-weighted citation impact, top 8% 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

13 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Adenosine stimulates the basolateral 50 pS KFrontiers in physiology · 2023
    Article
  3. Identification and function of adenosine A3 receptor in afferent arterioles.American journal of physiology. Renal physiology · 2015
    Article
  4. Renal autoregulation in health and disease.Physiological reviews · 2015
    Review
  5. Article
  6. Review
  7. Salt sensitivity of tubuloglomerular feedback in the early remnant kidney.American journal of physiology. Renal physiology · 2014
    Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. 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.

Mattias CarlströmDepartment of Medicine, Georgetown University Medical Center, Washington, District of Columbia, USA.
Christopher S Wilcox
William J Welch
Georgetown University · USGeorgetown University Medical Center · US

Funding

Renal Vascular Oxidative Stress in HypertensionP01HL068686 · NHLBI · GEORGETOWN UNIVERSITY · PI JOSE, PEDRO A., SANDBERG, KATHRYN L · 2001 to 2017
$28.8M
REGULATION OF RENAL FUNCTION AND BP BY THROMBOXANER37DK036079 · NIDDK · GEORGETOWN UNIVERSITY · PI WILCOX, CHRISTOPHER S · 2003 to 2012
$5.2M
NITRIC OXIDE SYNTHASE IN THE JUXTAGLOMERULAR APPARATUSR01DK049870 · NIDDK · GEORGETOWN UNIVERSITY · PI WILCOX, CHRISTOPHER S · 1994 to 2014
$4.6M
ADENOSINE RECEPTORS IN THE KIDNEYR01DK072183 · NIDDK · GEORGETOWN UNIVERSITY · PI WELCH, WILLIAM J · 2006 to 2015
$2.7M
NHLBI NIH HHS P01 HL068686NIDDK NIH HHS DK-072183NIDDK NIH HHS R01 DK049870NIDDK NIH HHS R01 DK072183NIDDK NIH HHS R37 DK036079
6 · The paper itself

Abstract

Adenosine can mediate the tubuloglomerular (TGF) response via activation of A(1) receptors on the afferent arteriole, but both adenosine A(1) and A(2) receptors can regulate preglomerular resistance. We tested the hypothesis that adenosine A(2) receptors offset the effect of A(1) receptors and modulate the TGF. Maximal TGF responses were measured in male Sprague-Dawley rats as changes in proximal stop-flow pressure (DeltaP(SF)) in response to increased perfusion of the loop of Henle (0 to 40 nl/min) with artificial tubular fluid (ATF). The maximal TGF response was studied after 5 min of intratubular perfusion (10 nl/min) with ATF alone, or with ATF plus the A(2A) receptor antagonist (ZM-241385; 10(-7) or 10(-5) mol/l), A(1) receptor antagonist (PSB-36; 10(-8) mol/l), or with a combination of A(1) (PSB-36; 10(-8) mol/l) and A(2A) (ZM-241385; 10(-7) mol/l) antagonists. The maximal TGF response (DeltaP(SF)) with ATF alone was 11.7 +/- 1.0 mmHg. Specific A(2) inhibition (low dose) enhanced the maximal TGF response (15.7 +/- 0.8 mmHg; P < 0.01), whereas a high dose (unspecific inhibition) attenuated the response (5.0 +/- 0.4 mmHg; P < 0.001). A(1) inhibition alone led to a paradoxical TGF response, with an increase in P(SF) of 3.1 +/- 0.5 mmHg (P < 0.05). Simultaneous application of A(1) and A(2) antagonists abolished the TGF response (DeltaP(SF): 0.4 +/- 0.3 mmHg). In conclusion, adenosine A(2) receptors modulate the TGF response by counteracting the effects of adenosine A(1) receptors.

Indexed as

MicrocirculationRenal CirculationAdenosineAdenosine A1 Receptor AntagonistsAdenosine A2 Receptor AntagonistsAnimalsArteriolesBlood PressureFeedback, PhysiologicalKidney GlomerulusKidney TubulesMalePerfusionRatsRats, Sprague-DawleyReceptor, Adenosine A11-butyl-8-(3-noradamantyl)-3-(3-hydroxypropyl)xanthineAdenosineAdenosine A1 Receptor AntagonistsAdenosine A2 Receptor AntagonistsReceptor, Adenosine A1Receptor, Adenosine A2ATriazinesTriazolesXanthinesZM 241385

Identifiers

PMID20519378
PMCPMC2928527
OpenAlexW2034373036

What OpenQuestion holds

Textmetadata
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.