ArticleAmerican journal of hypertension2002
Inhibition of inducible nitric oxide synthase during high dietary salt intake.
Article in American journal of hypertension, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 12 citations in OpenAlex.
- Amelioration of renal injury and oxidative stress by the nNOS inhibitor L-VNIO in the salt-sensitive mRen2.Lewis congenic rat.Journal of cardiovascular pharmacology · 2012Article
- Nitric oxide produced by endothelial nitric oxide synthase promotes diuresis.American journal of physiology. Regulatory, integrative and comparative physiology · 2010Article
- Inhibition of natriuretic factors increases blood pressure in rats.American journal of physiology. Renal physiology · 2009Article
- Deletion of inducible nitric oxide synthase provides cardioprotection in mice with 2-kidney, 1-clip hypertension.Hypertension (Dallas, Tex. : 1979) · 2009Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
backgroundPrevious studies indicate that nitric oxide (NO) is involved in the regulation of blood pressure (BP) and natriuresis in response to high sodium intake. We investigated the role of inducible NO synthase (iNOS) in response to an increased salt intake.
methodsConscious, chronically catheterized rats were exposed to a high-salt (6%) diet for 14 days while receiving vehicle or aminoguanidine ([AG]; 250 mg/kg/24 h), which selectively inhibits iNOS. A group of rats on normal salt intake + AG were also studied.
resultsAminoguanidine had no impact on BP (120 +/- 2 v 116 +/- 1 mm Hg, control v day 14) or 24-h urinary nitrite and nitrate excretion (UNOxV), in rats on normal salt but prevented lipopolysaccharide-induced hypotension. High salt alone had no impact on BP (120 +/- 1 v 121 +/- 1 mm Hg), whereas UNaV (1.3 +/- 0.2 v 3.5 +/- 0.6 microeq/min, P < .001) and UNOxV increased with high salt intake. The natriuretic response persisted (1.5 +/- 0.2 v 4.3 +/- 0.8 microeq/min, P < .005), but the increase in UNOXV was prevented with chronic AG although BP fell slightly (121 +/- 1 v 115 +/- 1 mm Hg, P < .05). There was no change in plasma volume with high salt, and 24-h UNaV increased appropriately in the presence of AG. The in vitro NOS activity was not increased in kidney homogenates by high salt diet, nor was it affected by chronic AG treatment.
conclusionWe conclude that NO from an iNOS source is not essential for the regulation of sodium excretion and BP in the presence of a high-salt diet in a normal rat.
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