Evidence map›Paper›PMID 41532628›Full record

ArticlePhysiological research2025

Combined RAS Modulation: The Effect on Plasma and Tissue Angiotensin Peptide Levels.

L Paulis, R Rajkovicova, K Repova, G Gubo, A Barta, M Poglitsch, O Domenig, N Andelova, M Ferko, O Pechanova and 1 more

Abstract read
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Article in Physiological research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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1 · What the graph read from it

What it found

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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

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

11 authors.

L PaulisInstitute of Pathophysiology, Faculty of Medicine, Comenius University, Bratislava, Slovak Republic.
R Rajkovicova
K Repova
G Gubo
A Barta
M Poglitsch
O Domenig
N Andelova
M Ferko
O Pechanova
F Simko

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Combined renin-angiotensin system (RAS) inhibition can enhance blood pressure control but has not improved clinical outcomes, underscoring the importance of complex changes in angiotensin peptide profiles in combined RAS blockade. We investigated hemodynamics and circulating and tissue angiotensin peptide profile in spontaneously hypertensive rats (SHR) treated with lisinopril, olmesartan and aliskiren and their dual combinations. SHR exhibited hypertension and left ventricular hypertrophy along with reduced circulating Ang I, Ang II, and Ang 1-7. Lisinopril produced the most pronounced antihypertensive effects, with additional reduction when combined with olmesartan or aliskiren. In contrast, aliskiren - either alone or in combination - had only modest effects in this low-RAS setting. The morphological changes of the myocardium largely mirrored the blood pressure responses across treatment groups, reinforcing the hemodynamic basis of structural remodeling in SHR. Lisinopril and olmesartan markedly increased Ang I and Ang 1-7, but lisinopril suppressed Ang II while olmesartan increased Ang II. Aliskiren further reduced Ang II and Ang 1-7. Across treatment strategies, dual RAS blockade frequently decreased both renal and circulating Ang 1-7 despite greater hemodynamic efficacy. Tissue analyses revealed minimal intrinsic Ang II synthesis in the left ventricle, consistent with AT?-dependent uptake of circulating Ang II, while renal peptide profiles indicated some local enzymatic activity with differential reliance on ACE and neprilysin. Our results advocate a cautious, mechanism-aware approach to combination RAS blockade and support therapeutic strategies that balance blood pressure lowering with preservation of the Ang 1-7 axis.

Indexed as

Angiotensin IAntihypertensive AgentsHypertensionPeptide FragmentsRenin-Angiotensin SystemAmidesAngiotensin II Type 1 Receptor BlockersAnimalsBlood PressureDrug Therapy, CombinationFumaratesImidazolesLisinoprilMaleRatsRats, Inbred SHRaliskirenAmidesAngiotensin Iangiotensin I (1-7)Angiotensin II Type 1 Receptor BlockersAntihypertensive AgentsFumaratesImidazolesLisinoprilolmesartanPeptide FragmentsTetrazoles

Identifiers

PMID41532628
PMCPMC12849780

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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.