Evidence map›Paper›PMID 23459599›Full record

ArticleAmerican journal of hypertension2013

Predominance of AT(1) blockade over mas-mediated angiotensin-(1-7) mechanisms in the regulation of blood pressure and renin-angiotensin system in mRen2.Lewis rats.

Jasmina Varagic, Sarfaraz Ahmad, Jessica L VonCannon, Norihito Moniwa, K Bridget Brosnihan, Jan Wysocki, Daniel Batlle, Carlos M Ferrario

Open access · bronzeAbstract read
In one paragraph

Article in American journal of hypertension, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
3.0field-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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.

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  15. Intracrine angiotensin II functions originate from noncanonical pathways in the human heart.American journal of physiology. Heart and circulatory physiology · 2016
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 2 countries.

Jasmina VaragicHypertension and Vascular Research Center, Wake Forest University, Winston-Salem, NC, USA. jvaragic@wfubmc.edu
Sarfaraz Ahmad
Jessica L VonCannon
Norihito Moniwa
K Bridget Brosnihan
Jan Wysocki
Daniel Batlle
Carlos M Ferrario
Wake Forest University · USNorthwestern University · US

Funding

Vaso-Hormonal Mechanisms in HypertensionP01HL051952 · NHLBI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI DELL'ITALIA, LOUIS J. · 1994 to 2019
$34.8M
NHLBI NIH HHS 2P01 HL-051952NHLBI NIH HHS P01 HL051952
6 · The paper itself

Abstract

backgroundWe investigated whether the antihypertensive actions of the angiotensin II (Ang II) receptor (AT(1)-R) blocker, olmesartan medoxomil, may in part be mediated by increased Ang-(1-7) in the absence of significant changes in plasma Ang II.

methodsmRen2.Lewis congenic hypertensive rats were administered either a vehicle (n = 14) or olmesartan (0.5 mg/kg/day; n = 14) by osmotic minipumps. Two weeks later, rats from both groups were further randomized to receive either the mas receptor antagonist A-779 (0.5 mg/kg/day; n = 7 per group) or its vehicle (n = 7 per group) for the next 4 weeks. Blood pressure was monitored by telemetry, and circulating and tissue components of the renin-angiotensin system (RAS) were measured at the completion of the experiments.

resultsAntihypertensive effects of olmesartan were associated with an increase in plasma renin concentration, plasma Ang I, Ang II, and Ang-(1-7), whereas serum aldosterone levels and kidney Ang II content were reduced. Preserved Ang-(1-7) content in kidneys was associated with increases of ACE2 protein but not activity and no changes on serum and kidney ACE activity. There was no change in cardiac peptide levels after olmesartan treatment. The antihypertensive effects of olmesartan were not altered by concomitant administration of the Ang-(1-7) receptor antagonist except for a mild further increase in plasma renin concentration.

conclusionsOur study highlights the independent regulation of RAS among plasma, heart, and kidney tissue in response to AT(1)-R blockade. Ang-(1-7) through the mas receptor does not mediate long-term effects of olmesartan besides counterbalancing renin release in response to AT(1)-R blockade.

Indexed as

AldosteroneAngiotensin IAngiotensin IIAngiotensin II Type 1 Receptor BlockersAnimalsAntihypertensive AgentsBlood PressureDisease Models, AnimalHypertensionImidazolesMaleOlmesartan MedoxomilPeptide FragmentsProto-Oncogene MasProto-Oncogene ProteinsRatsAldosteroneAngiotensin Iangiotensin I (1-7)Angiotensin IIAngiotensin II Type 1 Receptor BlockersAntihypertensive AgentsImidazolesOlmesartan MedoxomilPeptide FragmentsProto-Oncogene MasProto-Oncogene ProteinsReceptor, Angiotensin, Type 1Receptors, G-Protein-CoupledReninTetrazoles

Identifiers

PMID23459599
PMCPMC3657483
OpenAlexW2086781387

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.