Evidence map›Paper›PMID 21963837›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2011

A selective phosphodiesterase 3 inhibitor rescues low PO2-induced ATP release from erythrocytes of humans with type 2 diabetes: implication for vascular control.

Randy S Sprague, Elizabeth A Bowles, David Achilleus, Alan H Stephenson, Christopher G Ellis, Mary L Ellsworth

Erratum issuedAbstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.5field-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

20 citing papers in PubMed, 38 citations in OpenAlex.

  1. Trial
  2. Review
  3. Pannexin 1 channels control the hemodynamic response to hypoxia by regulating OAmerican journal of physiology. Heart and circulatory physiology · 2021
    Article
  4. Alteration of purinergic signaling in diabetes: Focus on vascular function.Journal of molecular and cellular cardiology · 2020
    Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Skeletal muscle vasodilation during systemic hypoxia in humans.Journal of applied physiology (Bethesda, Md. : 1985) · 2016
    Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Synergistic effects of C-peptide and insulin on low O2-induced ATP release from human erythrocytes.American journal of physiology. Regulatory, integrative and comparative physiology · 2013
    Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Review
4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

6 authors at 2 institutions in 2 countries.

Randy S SpragueDepartment of Pharmacological and Physiological Science, Saint Louis University School of Medicine, Missouri 63104, USA. spraguer@slu.edu
Elizabeth A Bowles
David Achilleus
Alan H Stephenson
Christopher G Ellis
Mary L Ellsworth
Saint Louis University · USWestern University · CA

Funding

Microvascular O2 Delivery: Impact of Erythrocyte-Released ATPR33HL089094 · NHLBI · SAINT LOUIS UNIVERSITY · PI ELLSWORTH, MARY L · 2007 to 2009
$1.6M
Microvascular O2 Delivery: Impact of Erythrocyte-Released ATPR33HL089125 · NHLBI · UNIVERSITY OF WESTERN ONTARIO · PI ELLIS, CHRISTOPHER G · 2007 to 2009
$621k
NHLBI NIH HHS HL-089094NHLBI NIH HHS HL-089125
6 · The paper itself

Abstract

Erythrocytes, via release of ATP in areas of low oxygen (O(2)) tension, are components of a regulatory system for the distribution of perfusion in skeletal muscle ensuring optimal O(2) delivery to meet tissue needs. In type 2 diabetes (DM2), there are defects in O(2) supply to muscle as well as a failure of erythrocytes to release ATP. The goal of this study was to ascertain if a phosphodiesterase 3 (PDE3) inhibitor, cilostazol, would rescue low O(2)-induced ATP release from DM2 erythrocytes and, thereby, enable these cells to dilate isolated erythrocyte-perfused skeletal muscle arterioles exposed to decreased extraluminal O(2). Erythrocytes were obtained from healthy humans (HH; n = 12) and humans with DM2 (n = 17). We determined that 1) PDE3B is similarly expressed in both groups, 2) mastoparan 7 (G(i) activation) stimulates increases in cAMP in HH but not in DM2 erythrocytes, and 3) pretreatment of DM2 erythrocytes with cilostazol resulted in mastoparan 7-induced increases in cAMP not different from those in HH cells. Most importantly, cilostazol restored the ability of DM2 erythrocytes to release ATP in response to low O(2). In contrast with perfusion with HH erythrocytes, isolated hamster retractor muscle arterioles perfused with DM2 erythrocytes constricted in response to low extraluminal PO(2). However, in the presence of cilostazol (100 μM), DM2 erythrocytes induced vessel dilation not different from that seen with HH erythrocytes. Thus rescue of low O(2)-induced ATP release from DM2 erythrocytes by cilostazol restored the ability of erythrocytes to participate in the regulation of perfusion distribution in skeletal muscle.

Indexed as

Adenosine TriphosphateAdultAnimalsArteriolesCase-Control StudiesCilostazolCricetinaeCyclic AMPCyclic Nucleotide Phosphodiesterases, Type 3Diabetes Mellitus, Type 2ErythrocytesFemaleHumansIntercellular Signaling Peptides and ProteinsMaleMesocricetusAdenosine TriphosphateCilostazolCyclic AMPCyclic Nucleotide Phosphodiesterases, Type 3Intercellular Signaling Peptides and ProteinsmastoparanOxygenPDE3B protein, humanPeptidesPhosphodiesterase 3 InhibitorsTetrazolesVasodilator AgentsWasp Venoms

Identifiers

PMID21963837
PMCPMC3233804
OpenAlexW2312885292

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.