Evidence map›Paper›PMID 20975035›Full record

ArticleHypertension (Dallas, Tex. : 1979)2010

Angiotensin II-mediated microvascular thrombosis.

Elena Y Senchenkova, Janice Russell, Lidiana D Almeida-Paula, Joseph W Harding, D Neil Granger

Open access · bronzeAbstract read
In one paragraph

Article in Hypertension (Dallas, Tex. : 1979), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
2.5field-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

59 citing papers in PubMed, 100 citations in OpenAlex.

  1. Associations Between PFA-Measured Aspirin Resistance, Platelet Count, Renal Function, and Angiotensin Receptor Blockers.Clinical and applied thrombosis/hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis/Hemostasis · 2018
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  7. Beyond pain relief: the thrombosis threat of celecoxib.Therapeutic advances in drug safety · 2025
    Article
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  9. Article
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  12. The Renin Angiotensin System as a Therapeutic Target in Traumatic Brain Injury.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023
    Review
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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

5 authors at 1 institution in 1 country.

Elena Y SenchenkovaDepartment of Molecular and Cellular Physiology, Louisiana State University Health Science Center, 1501 Kings Hwy, Shreveport, LA 71130-3932. dgrang@lsuhsc.edu.
Janice Russell
Lidiana D Almeida-Paula
Joseph W Harding
D Neil Granger
Washington State University · US

Funding

TRANSCAPILLARY FLUID EXCHANGER01HL026441 · NHLBI · UNIVERSITY OF SOUTH ALABAMA · PI GRANGER, D. NEIL · 1985 to 2013
$4.0M
NHLBI NIH HHS R01 HL026441NHLBI NIH HHS R01 HL26441-29
6 · The paper itself

Abstract

Hypertension is associated with an increased risk of thrombosis that appears to involve an interaction between the renin-angiotensin system and hemostasis. In this study we determined whether angiotensin II-mediated thrombosis occurs in arterioles and/or venules and assessed the involvement of type 1 (AT₁), type 2 (AT₂), and type 4 (AT₄) angiotensin II receptors, as well as receptors for endothelin 1 and bradykinin 1 and 2 in angiotensin II-enhanced microvascular thrombosis. Thrombus development in mouse cremaster microvessels was quantified after light/dye injury using the time of onset of the thrombus and time to blood flow cessation. Wild-type and AT₁ receptor-deficient mice were implanted with an angiotensin II-loaded ALZET pump for 2 weeks. Angiotensin II administration in both wild-type and ATAT₁ receptor-deficient mice significantly accelerated thrombosis in arterioles. Genetic deficiency and pharmacological antagonism of AT₁ receptors did not alter the thrombosis response to angiotensin II. Isolated murine platelets aggregated in response to low (picomolar) but not high (nanomolar) concentrations of angiotensin II. The platelet aggregation response to angiotensin II depended on AT₁ receptors. Antagonism of AT₂ receptors in vivo significantly prolonged the onset of angiotensin II-enhanced thrombosis, whereas an AT₄ receptor antagonist prolonged the time to flow cessation. Selective antagonism of either endothelin 1 or bradykinin 1 receptors largely prevented both the onset and flow cessation responses to chronic angiotensin II infusion. Our findings indicate that angiotensin II induced hypertension is accompanied by enhanced thrombosis in arterioles, and this response is mediated by a mechanism that involves AT₂, AT₄, bradykinin 1, and endothelin 1 receptor-mediated signaling.

Indexed as

Angiotensin IIAngiotensin Receptor AntagonistsAnimalsBradykinin Receptor AntagonistsEndothelin Receptor AntagonistsHypertensionMaleMiceMice, Inbred C57BLMicrovesselsPlatelet AggregationReceptors, AngiotensinReceptors, BradykininReceptors, EndothelinThrombosisAngiotensin IIAngiotensin Receptor AntagonistsBradykinin Receptor AntagonistsEndothelin Receptor AntagonistsReceptors, AngiotensinReceptors, BradykininReceptors, Endothelin

Identifiers

PMID20975035
PMCPMC3023299
OpenAlexW2149984223

What OpenQuestion holds

Textmetadata
LicenceTDM
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.