Maternal high-sodium intake affects the offspring' vascular renin-angiotensin system promoting endothelial dysfunction in rats.

Autor: Santos-Rocha J; Departamento de Fisiologia e Farmacologia, Universidade Federal de Pernambuco, Recife, Brazil., Lima-Leal GA; Departamento de Fisiologia e Farmacologia, Universidade Federal de Pernambuco, Recife, Brazil., Moreira HS; Departamento de Fisiologia e Farmacologia, Universidade Federal de Pernambuco, Recife, Brazil., Ramos-Alves FE; Departamento de Fisiologia e Farmacologia, Universidade Federal de Pernambuco, Recife, Brazil., de Sá FG; Departamento de Fisiologia e Farmacologia, Universidade Federal de Pernambuco, Recife, Brazil., Duarte GP; Departamento de Fisiologia e Farmacologia, Universidade Federal de Pernambuco, Recife, Brazil., Xavier FE; Departamento de Fisiologia e Farmacologia, Universidade Federal de Pernambuco, Recife, Brazil. Electronic address: fabianoxavier@ufpe.br.
Jazyk: angličtina
Zdroj: Vascular pharmacology [Vascul Pharmacol] 2019 Apr; Vol. 115, pp. 33-45. Date of Electronic Publication: 2019 Feb 18.
DOI: 10.1016/j.vph.2019.02.001
Abstrakt: Perinatal sodium overload induces endothelial dysfunction in adult offspring, but the underlying mechanisms are not fully known. The involvement of tissue renin-angiotensin system on high sodium-programmed endothelial dysfunction was examined. Acetylcholine and angiotensin I and II responses were analyzed in aorta and mesenteric resistance arteries from 24-week-old male offspring of normal-salt (O-NS, 1.3% NaCl) and high-salt (O-HS, 8% NaCl) fed dams. COX-2 expression, O 2 - production and angiotensin converting enzyme (ACE) activity were determined. A separated O-HS was treated with losartan (15 mg kg -1 /day) for eight weeks. Compared to O-NS, O-HS were normotensive. Acetylcholine-induced relaxation was impaired in O-HS arteries, which was improved by tempol, apocynin or indomethacin. The angiotensin I-induced contraction was greater in O-HS arteries, whereas the angiotensin II responses were unchanged. ACE activity, O 2 - production and COX-2 expression were increased in O-HS arteries. In this group, the increased O 2 - production was inhibited by apocynin or losartan. Chronic losartan decreased COX-2 expression and restored the endothelium-dependent vasodilation in O-HS. Our findings reiterate that perinatal sodium overload programs endothelial dysfunction in adult offspring through a blood pressure-independent mechanism. Our results also suggest that vascular angiotensin II is the main mediator of high sodium-programmed endothelial dysfunction, promoting COX-2 expression and oxidative stress.
(Copyright © 2019 Elsevier Inc. All rights reserved.)
Databáze: MEDLINE
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