Naslov
Dietary salt intake, endothelial function, and cascular oxidant stress: parallel lessons from humans and animals

Autori
Lombard, JH ; Durand, M ; Priestley, J ; Raffai, G ; Baer, A ; Drenjancevic, I ; Zhu, J

Vrsta, podvrsta i kategorija rada
Sažeci sa skupova, sažetak, znanstveni

Izvornik
Selected abstracts of the 2nd International Symposium on Hypertension Osijek ; u: Kidney and Blood Pressure Research 33 (2010) (6)413-441 ; 6 / Drenjančević, Ines ; Jelaković, Bojan ; Koller, Akos - : Karger Publishers, 2010, 424-424

ISBN
978-3-8055-8396-1

Skup
Second International Symposium on Hypertension Translational Medicine in Hypertension

Mjesto i datum
Osijek, Hrvatska, 18.11.2010. - 21.11.2010

Vrsta sudjelovanja
Predavanje

Vrsta recenzije
Međunarodna recenzija

Ključne riječi
salt intake; endothelium; vascular oxidant stress

Sažetak
Introduction: There is growing evidence that elevated dietary salt intake can contribute to endothelial dysfunction and increased mortality in humans. Experimental animal models that recapitulate the effects of elevated dietary salt intake in humans can be tremendously valuable in elucidating the mechanisms of endothelial dysfunction in salt-sensitive hypertension. Methods: The responses of arteries to multiple vasodilator stimuli were evaluated in isolated cannulated resistance arteries, in situ arterioles, and aortic rings. Nitric oxide (NO) availability and superoxide levels were assessed with using DAF-2 and DHE staining, respectively. Studies were conducted in normotensive rats and hamsters, Dahl salt sensitive (SS) rats, and in consomic and congenic rat strains having the Brown Norway (BN) renin allele substituted into the Dahl SS genetic background. Animals were fed either a low-salt (LS ; 0.4% NaCl) or high salt (HS ; 4% NaCl) diet. Results: Vascular relaxation in response to multiple vasodilator stimuli was impaired in animals switched to HS diet, and in Dahl SS rats fed LS diet, which exhibit chronically low angiotensin II levels due to an inability to regulate their plasma renin activity normally. Impaired vascular relaxation was paralleled by reduced NO levels and elevated superoxide levels. Vascular relaxation could be restored by chronic i.v. infusion of a subpressor dose of angiotensin II and by antioxidant treatment. Substitution of the BN renin allele into the SS genetic background also restored salt-sensitive vascular relaxation. Conclusions: The deleterious effects of elevated dietary salt intake and lower than normal levels of circulating angiotensin II have been demonstrated in multiple normotensive animals, and in genetic models of salt sensitive hypertension such as the Dahl SS rat. The availability of multiple experimental animal models promises to provide crucial insight into the effects of elevated dietary salt intake and the mechanisms of early cardiovascular dysfunction in salt-sensitive humans.

Izvorni jezik
Engleski

Znanstvena područja
Temeljne medicinske znanosti

Napomena
DOI: 10.1159/000321436. Svi sazeci sa Skupa objavljeni su u Kidney & blood pressure research (ISSN 1423-0143) 30 (2007) (1) ISBN 978-3-8055-8396-1.

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