Evidence map›Paper›PMID 27324312›Full record

ReviewThe Journal of physiology2016

Arteriolar oxygen reactivity: where is the sensor and what is the mechanism of action?

William F Jackson

Open access · greenAbstract readReview
In one paragraph

Review in The Journal of physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
2.7field-weighted citation impact, top 10% 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

29 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Hyperoxia and acute brain injury.Critical care (London, England) · 2025
    Article
  4. Article
  5. Article
  6. Hif1α-dependent mitochondrial acute ONature communications · 2024
    Article
  7. Article
  8. Electro-metabolic signaling.The Journal of general physiology · 2024
    Article
  9. Article
  10. Vascular mechanotransduction.Physiological reviews · 2023
    Review
  11. Review
  12. Could respiration-driven blood oxygen changes modulate neural activity?Pflugers Archiv : European journal of physiology · 2023
    Review
  13. Article
  14. Review
  15. Article
  16. Sympathetic neurovascular transduction following acute hypoxia.Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2021
    Article
  17. Article
  18. Article
  19. Review
  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

1 author at 1 institution in 1 country.

William F JacksonDepartment of Pharmacology and Toxicology, Michigan State University, East Lansing, MI, 48824, USA. jacks783@msu.edu.
Michigan State University · US

Funding

SIGNALING MECHANISMS IN ARTERIES AND VEINS IN HYPERTENSIONP01HL070687 · NHLBI · MICHIGAN STATE UNIVERSITY · PI WATTS, STEPHANIE W · 2003 to 2019
$22.8M
CONTROL OF MICROVASCULAR FUNCTION BY OXYGENR01HL032469 · NHLBI · WESTERN MICHIGAN UNIVERSITY · PI JACKSON, WILLIAM F. · 1987 to 2006
$1.1M
NHLBI NIH HHS P01 HL070687NHLBI NIH HHS R01 HL032469
6 · The paper itself

Abstract

Arterioles in the peripheral microcirculation are exquisitely sensitive to changes in PO2 in their environment: increases in PO2 cause vasoconstriction while decreases in PO2 result in vasodilatation. However, the cell type that senses O2 (the O2 sensor) and the signalling pathway that couples changes in PO2 to changes in arteriolar tone (the mechanism of action) remain unclear. Many (but not all) ex vivo studies of isolated cannulated resistance arteries and large, first-order arterioles support the hypothesis that these vessels are intrinsically sensitive to PO2 with the smooth muscle, endothelial cells, or red blood cells serving as the O2 sensor. However, in situ studies testing these hypotheses in downstream arterioles have failed to find evidence of intrinsic O2 sensitivity, and instead have supported the idea that extravascular cells sense O2 . Similarly, ex vivo studies of isolated, cannulated resistance arteries and large first-order arterioles support the hypotheses that O2 -dependent inhibition of production of vasodilator cyclooxygenase products or O2 -dependent destruction of nitric oxide mediates O2 reactivity of these upstream vessels. In contrast, most in vivo studies of downstream arterioles have disproved these hypotheses and instead have provided evidence supporting the idea that O2 -dependent production of vasoconstrictors mediates arteriolar O2 reactivity, with significant regional heterogeneity in the specific vasoconstrictor involved. Oxygen-induced vasoconstriction may serve as a protective mechanism to reduce the oxidative burden to which a tissue is exposed, a process that is superimposed on top of the local mechanisms which regulate tissue blood flow to meet a tissue's metabolic demand.

Indexed as

AnimalsArteriolesEndothelial CellsErythrocytesHumansHydroxyeicosatetraenoic AcidsLeukotrienesMast CellsMyocytes, Smooth MuscleNitric OxideOxygenProstaglandinsSuperoxidesVasoconstriction20-hydroxy-5,8,11,14-eicosatetraenoic acidHydroxyeicosatetraenoic AcidsLeukotrienesNitric OxideOxygenProstaglandinsSuperoxidesarteriolesmicrocirculationoxygenoxygen sensingvasoconstrictionvasodilatation

Identifiers

PMID27324312
PMCPMC5023707
OpenAlexW2474870885

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.