Evidence map›Paper›PMID 20359465›Full record

ArticleBiochemical pharmacology2010

An activated renin-angiotensin system maintains normal blood pressure in aryl hydrocarbon receptor heterozygous mice but not in null mice.

Nan Zhang, Larry N Agbor, Jason A Scott, Tyler Zalobowski, Khalid M Elased, Alicia Trujillo, Melissa Skelton Duke, Valerie Wolf, Mary T Walsh, Jerry L Born and 5 more

Open access · greenAbstract read
In one paragraph

Article in Biochemical pharmacology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
3.0field-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

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.

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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

15 authors at 2 institutions in 1 country.

Nan ZhangDepartment of Pharmaceutical Sciences, University of New Mexico Health Sciences Center, Albuquerque, 87131, USA.
Larry N Agbor
Jason A Scott
Tyler Zalobowski
Khalid M Elased
Alicia Trujillo
Melissa Skelton Duke
Valerie Wolf
Mary T Walsh
Jerry L Born
Linda A Felton
Jian Wang
Wei Wang
Nancy L Kanagy
Mary K Walker
University of New Mexico · USWright State University · US

Funding

Ah Receptor and Endothelin-Dependent HypertensionR01HL078914 · NHLBI · UNIVERSITY OF NEW MEXICO · PI WALKER, MARY K · 2006 to 2010
$1.9M
NHLBI NIH HHS R01 HL078914
6 · The paper itself

Abstract

It has been postulated that fetal vascular abnormalities in aryl hydrocarbon receptor null (ahr(-/-)) mice may alter cardiovascular homeostasis in adulthood. We tested the hypothesis that blood pressure regulation in adult heterozygous mice (ahr(+/-)) would be normal, compared to ahr(-/-) mice, since no vascular abnormalities have been reported in the heterozygote animals. Mean arterial blood pressure (MAP) was measured using radiotelemetry prior to and during treatment with inhibitors of the autonomic nervous system, nitric oxide synthase (NOS), angiotensin converting enzyme (ACE), or endothelin-1 A receptor (ET(A)). Also, indices of renin-angiotensin system (RAS) activation were measured. ahr(+/-) and ahr(-/-) mice were normotensive and hypotensive, respectively, compared to wild-type (ahr(+/+)) littermates. Responses of all genotypes to autonomic nervous system inhibition were normal. ahr(+/-) mice responded normally to NOS inhibition, while the responses of ahr(-/-) mice were significantly blunted. In contrast, ahr(+/-) mice were significantly more responsive to inhibition of ACE, an ET(A) antagonist, or both, while ahr(-/-) mice were significantly less responsive to ACE inhibition and more responsive to an ET(A) antagonist. ahr(+/-) mice also exhibited significant increases in plasma renin and ACE activity, plasma sodium, and urine osmolality, indicative of RAS activation. Thus, normotension in ahr(+/-) mice appears to be maintained by increased RAS and ET-1 signaling, while hypotension in ahr(-/-) mice may result from decreased RAS signaling. In conclusion, despite the lack of overt fetal vascular abnormalities in ahr(+/-) mice, the loss of a single ahr allele has a significant effect on blood pressure regulation.

Indexed as

Angiotensin-Converting Enzyme InhibitorsAngiotensin IIAnimalsAntihypertensive AgentsAorta, ThoracicBlood PressureDioxolesEndothelin A Receptor AntagonistsFemaleHeart RateHeterozygoteMaleMiceMice, KnockoutNitric Oxide SynthasePeptidyl-Dipeptidase AAngiotensin-Converting Enzyme InhibitorsAngiotensin IIAntihypertensive AgentsDioxolesEndothelin A Receptor AntagonistsNitric Oxide SynthasePD 155080Peptidyl-Dipeptidase AReceptor, Endothelin AReceptors, Aryl Hydrocarbon

Identifiers

PMID20359465
PMCPMC2867364
OpenAlexW2000898620

What OpenQuestion holds

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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.