Evidence map›Paper›PMID 24321189›Full record

ArticleVascular pharmacology2014

Enhanced angiotensin-converting enzyme activity and systemic reactivity to angiotensin II in normotensive rats exposed to a high-sodium diet.

Sandra Crestani, Arquimedes Gasparotto Júnior, Maria C A Marques, Jennifer C Sullivan, R Clinton Webb, J Eduardo da Silva-Santos

Abstract read
In one paragraph

Article in Vascular pharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
–field-weighted citation impact
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

14 citing papers in PubMed.

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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

6 authors.

Sandra CrestaniDepartment of Pharmacology, Universidade Federal do Paraná, Curitiba, PR, Brazil; Department of Physiology, Georgia Health Sciences University, Augusta, GA, USA.
Arquimedes Gasparotto JúniorInstitute of Biological Sciences, Medical and Health, Universidade Paranaense, Umuarama, PR, Brazil.
Maria C A MarquesDepartment of Pharmacology, Universidade Federal do Paraná, Curitiba, PR, Brazil.
Jennifer C SullivanDepartment of Medicine, Georgia Health Sciences University, Augusta, GA, USA.
R Clinton WebbDepartment of Physiology, Georgia Health Sciences University, Augusta, GA, USA.
J Eduardo da Silva-SantosDepartment of Pharmacology, Universidade Federal do Paraná, Curitiba, PR, Brazil; Laboratory of Cardiovascular Pharmacology, Department of Pharmacology, Universidade Federal de Santa Catarina, Florianópolis, SC, Brazil. Electronic address: j.e.silva.santos@ufsc.br.

Funding

Nitric Oxide Inhibits RhoA/Rho-kinase in Penile ErectionR01HL071138 · NHLBI · MEDICAL COLLEGE OF GEORGIA (MCG) · PI WEBB, R CLINTON · 2003 to 2011
$2.9M
NHLBI NIH HHS R01 HL071138NHLBI NIH HHS R01HL071138
6 · The paper itself

Abstract

A high salt diet is associated with reduced activity of the renin-angiotensin-aldosterone system (RAAS). However, normotensive rats exposed to high sodium do not show changes in systemic arterial pressure. We hypothesized that, despite the reduced circulating amounts of angiotensin II induced by a high salt diet, the cardiovascular system's reactivity to angiotensin II is increased in vivo, contributing to maintain arterial pressure at normal levels. Male Wistar rats received chow containing 0.27% (control), 2%, 4%, or 8% NaCl for six weeks. The high-sodium diet did not lead to changes in arterial pressure, although plasma levels of angiotensin II and aldosterone were reduced in the 4% and 8% NaCl groups. The 4% and 8% NaCl groups showed enhanced pressor responses to angiotensin I and II, accompanied by unchanged and increased angiotensin-converting enzyme activity, respectively. The 4% NaCl group showed increased expression of angiotensin II type 1 receptors and reduced expression of angiotensin II type 2 receptors in the aorta. In addition, the hypotensive effect of losartan was reduced in both 4% and 8% NaCl groups. In conclusion these results explain, at least in part, why the systemic arterial pressure is maintained at normal levels in non-salt sensitive and healthy rats exposed to a high salt diet, when the functionality of RAAS appears to be blunted, as well as suggest that angiotensin II has a crucial role in the vascular dysfunction associated with high salt intake, even in the absence of hypertension.

Indexed as

AldosteroneAngiotensin IAngiotensin IIAngiotensin II Type 1 Receptor BlockersAnimalsAortaBlood PressureLosartanMaleRatsRats, WistarReceptor, Angiotensin, Type 1Renin-Angiotensin SystemSodium Chloride, DietaryAldosteroneAngiotensin IAngiotensin IIAngiotensin II Type 1 Receptor BlockersLosartanReceptor, Angiotensin, Type 1Sodium Chloride, DietaryAngiotensin II receptorsArterial pressureHigh saltLosartanVascular reactivity

Identifiers

PMID24321189
PMCPMC5560024

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Registered trials

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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.