Low-dose angiotensin II supplementation restores flow-induced dilation mechanisms in cerebral arteries of Sprague-Dawley rats on a high salt diet.


Journal

Journal of hypertension
ISSN: 1473-5598
Titre abrégé: J Hypertens
Pays: Netherlands
ID NLM: 8306882

Informations de publication

Date de publication:
01 03 2022
Historique:
pubmed: 1 12 2021
medline: 24 3 2022
entrez: 30 11 2021
Statut: ppublish

Résumé

Salt-induced suppression of angiotensin II contributes to impaired endothelium-dependent vascular reactivity. The present study investigated the effect of chronic low-dose angiotensin II (ANG II) supplementation on the mechanisms of flow-induced dilation (FID) and oxidative stress at the cellular and molecular level in middle cerebral arteries (MCA) of male Sprague-Dawley rats fed high salt diet. Rats (10 weeks old) were randomly assigned to a low salt diet group (0.4% NaCl in rat chow); high salt diet group (7 days 4% NaCl in rat chow) or HS+ANG II group [7 days high salt diet with 3 days ANG II administration via osmotic minipumps (100 ng/kg per min on days 4-7)]. FID was determined in absence/presence of the NOS inhibitor L-NAME, the non-selective cyclooxygenase (COX-1,2) inhibitor indomethacin, a selective inhibitor of CYP450 epoxygenase activity (MS-PPOH) and the superoxide dismutase mimetic TEMPOL. Gene expression of antioxidative enzymes, and of genes and proteins involved in FID mechanisms were determined by RT-qPCR and western blot. Vascular nitric oxide and superoxide/reactive oxygen species levels were assessed by direct fluorescence. Serum systemic oxidative stress parameters were measured by spectrophotometry. Chronic low-dose ANG II supplementation in high salt fed rats restored FID of MCAs, which was nitric oxide, prostanoid and epoxyeicosatrienoic acid dependent. ANG II changed the protein/gene expression of COXs, HIF-1α and VEGF and significantly increased GPx4 and EC-SOD antioxidative enzyme expression, decreased systemic oxidative stress, decreased superoxide/ROS levels and increased nitric oxide bioavailability in the vascular wall. Physiological levels of circulating ANG II are crucial to maintain the HIF-1α dependent mechanisms of FID and vascular oxidative balance without affecting mean arterial pressure.

Identifiants

pubmed: 34845157
doi: 10.1097/HJH.0000000000003030
pii: 00004872-202203000-00005
doi:

Substances chimiques

Angiotensin II 11128-99-7
Sodium Chloride 451W47IQ8X

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

441-452

Informations de copyright

Copyright © 2021 Wolters Kluwer Health, Inc. All rights reserved.

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Auteurs

Anita Matic (A)

Institute and Department of Physiology and Immunology, Faculty of Medicine Osijek, Josip Juraj Strosssmayer University of Osijek.
Scientific Centre of Excellence for Personalized Health Care, University of Josip Juraj Strossmayer University of Osijek.

Ivana Jukic (I)

Institute and Department of Physiology and Immunology, Faculty of Medicine Osijek, Josip Juraj Strosssmayer University of Osijek.
Scientific Centre of Excellence for Personalized Health Care, University of Josip Juraj Strossmayer University of Osijek.

Zrinka Mihaljevic (Z)

Institute and Department of Physiology and Immunology, Faculty of Medicine Osijek, Josip Juraj Strosssmayer University of Osijek.
Scientific Centre of Excellence for Personalized Health Care, University of Josip Juraj Strossmayer University of Osijek.

Nikolina Kolobaric (N)

Institute and Department of Physiology and Immunology, Faculty of Medicine Osijek, Josip Juraj Strosssmayer University of Osijek.
Scientific Centre of Excellence for Personalized Health Care, University of Josip Juraj Strossmayer University of Osijek.

Ana Stupin (A)

Institute and Department of Physiology and Immunology, Faculty of Medicine Osijek, Josip Juraj Strosssmayer University of Osijek.
Scientific Centre of Excellence for Personalized Health Care, University of Josip Juraj Strossmayer University of Osijek.
Department of Pathophysiology, Physiology and Immunology, Faculty of Dental Medicine and Health Osijek, Josip Juraj Strossmayer University of Osijek, Osijek.

Natasa Kozina (N)

Institute and Department of Physiology and Immunology, Faculty of Medicine Osijek, Josip Juraj Strosssmayer University of Osijek.

Ivana Tartaro Bujak (IT)

Radiation Chemistry and Dosimetry Laboratory, Ruđer Bošković Institute, Zagreb.

Aleksandar Kibel (A)

Institute and Department of Physiology and Immunology, Faculty of Medicine Osijek, Josip Juraj Strosssmayer University of Osijek.
Scientific Centre of Excellence for Personalized Health Care, University of Josip Juraj Strossmayer University of Osijek.
Internal Clinic, Osijek University Hospital, Osijek, Croatia.

Julian H Lombard (JH)

Department of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin, USA.

Ines Drenjancevic (I)

Institute and Department of Physiology and Immunology, Faculty of Medicine Osijek, Josip Juraj Strosssmayer University of Osijek.
Scientific Centre of Excellence for Personalized Health Care, University of Josip Juraj Strossmayer University of Osijek.

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