Evidence map›Paper›PMID 35740253›Full record

ArticleBiomedicines2022

Vasoconstrictor and Pressor Effects of Des-Aspartate-Angiotensin I in Rat.

Rosemary Wangensteen, Manuel Gómez-Guzmán, Inmaculada Banegas, Isabel Rodríguez-Gómez, Rosario Jiménez, Juan Duarte, Joaquín García-Estañ, Félix Vargas

Open access · goldAbstract read
In one paragraph

Article in Biomedicines, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact, top 88% 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

0 citing papers in PubMed, 0 citations in OpenAlex.

No citing paper in PubMed yet.

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

8 authors at 3 institutions in 1 country.

Rosemary WangensteenArea of Physiology, Department of Health Sciences, University of Jaén, 23071 Jaén, Spain.ORCID 0000-0001-7161-9925
Manuel Gómez-GuzmánDepartment of Pharmacology, University of Granada, 18071 Granada, Spain.ORCID 0000-0003-2452-9286
Inmaculada BanegasArea of Physiology, Department of Health Sciences, University of Jaén, 23071 Jaén, Spain.ORCID 0000-0002-1910-3726
Isabel Rodríguez-GómezDepartment of Physiology, University of Granada, 18071 Granada, Spain.
Rosario JiménezDepartment of Pharmacology, University of Granada, 18071 Granada, Spain.ORCID 0000-0003-3872-2669
Juan DuarteDepartment of Pharmacology, University of Granada, 18071 Granada, Spain.ORCID 0000-0002-9153-5857
Joaquín García-EstañDepartment of Physiology, Faculty of Medicine, IMIB, University of Murcia, 30120 Murcia, Spain.ORCID 0000-0002-7243-0240
Félix VargasDepartment of Physiology, University of Granada, 18071 Granada, Spain.
Universidad de Granada · ESUniversidad de Jaén · ESUniversidad de Murcia · ES

Funding

Carlos III Health Institute of Spain PI18/01715Red de Investigación Renal RedInRen. "FEDER una manera de hacer Europa". RD16/0009/0033
6 · The paper itself

Abstract

This study investigated the vasoactive effects of des-aspartate-angiotensin-I (DAA-I) in male Wistar rats on whole body vascular bed, isolated perfused kidneys, and aortic rings. Dose-response curves to DAA-I were compared with those to angiotensin II (Ang II). The Ang II-type-1 (AT1) receptor blocker, losartan, was used to evaluate the role of AT1 receptors in the responses to DAA-I. Studies were also conducted of the responsiveness in aortic rings after endothelium removal, nitric oxide synthase inhibition, or AT2 receptor blockade. DAA-I induced a dose-related systemic pressor response that was shifted to the right compared with Ang II. Losartan markedly attenuated the responsiveness to DAA-I. DAA-I showed a similar pattern in renal vasculature and aortic rings. In aortic rings, removal of endothelium and nitric oxide inhibition increased the sensitivity and maximal response to DAA-I and Ang II. AT2 receptor blockade did not significantly affect the responsiveness to DAA-I. According to these findings, DAA-I increases the systemic blood pressure and vascular tone in conductance and resistance vessels via AT1 receptor activation. This vasoconstrictor effect of DAA-I participates in the homeostatic control of arterial pressure, which can also contribute to the pathogenesis of hypertension. DAA-I may therefore be a potential therapeutic target in cardiovascular disease.

Indexed as

des-aspartate-angiotensin Ihypertensionkidneyrenin-angiotensin systemvascular reactivity

Identifiers

PMID35740253
PMCPMC9220223
OpenAlexW4281492364

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.