Evidence map›Paper›PMID 21940850›Full record

ArticleJournal of applied physiology (Bethesda, Md. : 1985)2011

Functional contribution of P2Y1 receptors to the control of coronary blood flow.

Shawn B Bender, Zachary C Berwick, M Harold Laughlin, Johnathan D Tune

Abstract read
In one paragraph

Article in Journal of applied physiology (Bethesda, Md. : 1985), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.8field-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

16 citing papers in PubMed, 32 citations in OpenAlex.

  1. Review
  2. Unraveling the Gordian knot of coronary pressure-flow autoregulation.Journal of molecular and cellular cardiology · 2024
    Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. The role of purinergic P2YPurinergic signalling · 2020
    Article
  8. Review
  9. Article
  10. Article
  11. Regulation of Coronary Blood Flow.Comprehensive Physiology · 2017
    Review
  12. Review
  13. Article
  14. Article
  15. Effect of extraluminal ATP application on vascular tone and blood flow in skeletal muscle: implications for exercise hyperemia.American journal of physiology. Regulatory, integrative and comparative physiology · 2013
    Article
  16. 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.

Shawn B BenderDept. of Biomedical Sciences, Univ. of Missouri, Columbia, MO 65211, USA. benders@missouri.edu
Zachary C Berwick
M Harold Laughlin
Johnathan D Tune
Indiana University School of MedicineUniversity of Missouri · US

Funding

Vascular Biology: Exercise Training and Vascular DiseaseP01HL052490 · NHLBI · UNIVERSITY OF MISSOURI-COLUMBIA · PI LAUGHLIN, M HAROLD · 1995 to 2010
$19.3M
NHLBI NIH HHS HL-092245NHLBI NIH HHS HL-52490
6 · The paper itself

Abstract

Activation of ADP-sensitive P2Y(1) receptors has been proposed as an integral step in the putative "nucleotide axis" regulating coronary blood flow. However, the specific mechanism(s) and overall contribution of P2Y(1) receptors to the control of coronary blood flow have not been clearly defined. Using vertically integrative studies in isolated coronary arterioles and open-chest anesthetized dogs, we examined the hypothesis that P2Y(1) receptors induce coronary vasodilation via an endothelium-dependent mechanism and contribute to coronary pressure-flow autoregulation and/or ischemic coronary vasodilation. Immunohistochemistry revealed P2Y(1) receptor expression in coronary arteriolar endothelial and vascular smooth muscle cells. The ADP analog 2-methylthio-ADP induced arteriolar dilation in vitro and in vivo that was abolished by the selective P2Y(1) antagonist MRS-2179 and the nitric oxide synthase inhibitor N(G)-nitro-l-arginine methyl ester. MRS-2179 did not alter baseline coronary flow in vivo but significantly attenuated coronary vasodilation to ATP in vitro and in vivo and the nonhydrolyzable ATP analog ATPγS in vitro. Coronary blood flow responses to alterations in coronary perfusion pressure (40-100 mmHg) or to a brief 15-s coronary artery occlusion were unaffected by MRS-2179. Our data reveal that P2Y(1) receptors are functionally expressed in the coronary circulation and that activation produces coronary vasodilation via an endothelium/nitric oxide-dependent mechanism. Although these receptors represent a critical component of purinergic coronary vasodilation, our findings indicate that P2Y(1) receptor activation is not required for coronary pressure-flow autoregulation or reactive hyperemia.

Indexed as

Adenosine DiphosphateAdenosine TriphosphateAnimalsArteriolesBlood Flow VelocityCoronary CirculationDogsHyperemiaIn Vitro TechniquesMalePurinergic P2Y Receptor AgonistsPurinergic P2Y Receptor AntagonistsReceptors, Purinergic P2Y1ThionucleotidesVasodilationadenosine 5'-O-(3-thiotriphosphate)Adenosine DiphosphateAdenosine Triphosphatemethylthio-ADPN(6)-methyl-2'-deoxyadenosine 3',5'-diphosphatePurinergic P2Y Receptor AgonistsPurinergic P2Y Receptor AntagonistsReceptors, Purinergic P2Y1Thionucleotides

Identifiers

PMID21940850
PMCPMC3233891
OpenAlexW1989336517

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.