Evidence map›Paper›PMID 36845669›Full record

ArticleJournal of the renin-angiotensin-aldosterone system : JRAAS2023

Polymorphisms in the Renin-Angiotensin System and eNOS Glu298Asp Genes Are Associated with Increased Risk for Essential Hypertension in a Mexican Population.

Irma Isordia-Salas, David Santiago-Germán, Alejandro Flores-Arizmendi, Alfredo Leaños-Miranda

Abstract read
In one paragraph

Article in Journal of the renin-angiotensin-aldosterone system : JRAAS, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
–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

12 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Association BetweenInternational journal of environmental research and public health · 2026
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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

4 authors.

Irma Isordia-SalasThrombosis, Hemostasis and Atherogenesis Research Unit, H.G.R. No. 1 Dr. "Carlos Mac Gregor Sánchez Navarro", Mexican Social Security Institute, México City, Mexico.ORCID https://orcid.org/0000-0002-8986-2330
David Santiago-GermánHealth Research Division, Highly Specialized Medical Unit of Traumatology, Orthopedics and Rehabilitation "Dr. Victorio de la Fuente Narváez", Mexican Social Security Institute, Mexico City, Mexico.ORCID https://orcid.org/0000-0002-6145-970X
Alejandro Flores-ArizmendiHemodynamic Department, National Medical Center, Institute of Security and Social Services for State Workers, Mexico City, Mexico.ORCID https://orcid.org/0000-0003-0402-3421
Alfredo Leaños-MirandaMedical Research Unit in Reproductive Medicine, Highly Specialized Medical Unit No. 4, Mexican Social Security Institute, Mexico City, Mexico.ORCID https://orcid.org/0000-0002-8848-5000

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Essential hypertension is the result of modifiable and genetic factors, and it is associated with increased risk for atherothrombosis. Some polymorphisms are associated with hypertensive disease. The objective was to analyze the association between eNOS Glu298Asp, MTHR C677T, AGT M235T, AGT T174M, and A1166C and ACE I/D polymorphisms with essential hypertension in the Mexican population. Materials and Methods: In the present study, 224 patients with essential hypertension and 208 subjects without hypertension were included. The Glu298Asp, C677T, M235T, T174M, A1166C, and I/D polymorphisms were determined by the PCR-RFLP technique. Results: We found statistical differences in age, gender, BMI, systolic and diastolic blood pressure, and total cholesterol between control and cases. However, we found no significant differences in HbA1c and triglycerides between both groups. We observed statistical significant differences in the genotype distribution of Glu298Asp ( Conclusions: We identified that Glu298Asp, I/D, and M234T polymorphisms represented an increased risk for essential hypertension and those genetic variants could contribute to the presence of endothelial dysfunction and vasopressor effect, hyperplasia, and hypertrophy of smooth muscle cells, which had an impact for hypertension. In contrast, we found no association between C677C, M174T, and A1166C polymorphisms and hypertensive disease. We suggested that those genetic variants could be identified in individuals with high risk to avoid hypertension and thrombotic disease.

Indexed as

HypertensionRenin-Angiotensin SystemAngiotensinogenEssential HypertensionGenotypeHumansNitric Oxide Synthase Type IIINorth American PeoplePeptidyl-Dipeptidase APolymorphism, GeneticPolymorphism, Restriction Fragment LengthAngiotensinogenNitric Oxide Synthase Type IIINOS3 protein, humanPeptidyl-Dipeptidase A

Identifiers

PMID36845669
PMCPMC9957645

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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.