Research article summary (published May 2009):

Whole-body basal nitric oxide production is impaired in postprandial endothelial dysfunction in healthy rats.

Full Abstract

In healthy humans, a high-saturated-fat/high-sucrose meal induces vascular endothelial dysfunction, a hallmark of atherogenesis. This transient dysfunction indicates a loss in nitric oxide (NO) production and/or bioactivity in the vasculature but it remains unknown if this is the local manifestation of a general impairment in NO pathway in the postprandial state. Here, we studied whole-body NO production and systemic NO bioactivity in postprandial endothelial dysfunction, as induced by a high-saturated-fat, high-sucrose meal. We first developed a physiological test of endothelial function on conscious rats, based on the transient fall in blood pressure after iv acetylcholine, and showed that this response was NO-dependent. As assessed with this method in healthy rats, endothelial function decreased during the postprandial state, being 60+/-7% lower than baseline at 6h after the meal challenge, associated with important elevations in plasma triglycerides and hydroperoxides. Aortic superoxide anion production, as assessed by oxidative fluorescent detection, was higher 6h after the meal challenge than after the nutrients vehicle (water). During the postprandial period, plasma cGMP, but not plasma ANP, markedly decreased, indicating a general decrease in NO bioavailability, which was numerically maximal 4h after the meal challenge. As determined 4h after ingestion by a tracer-based method using iv [(15)N(2)-(guanido)]-arginine, the whole-body NO production fell by 27+/-9% postprandially. This is the first study evidencing that a meal challenge that impairs the stimulated, NO-mediated, vascular response also reduces whole-body basal NO production and bioavailability. Postprandial pathophysiology may build on this general, fundamental alteration in NO production.

Author information

Author/s: Magné, Joëlle (J); Huneau, Jean François (JF); Delemasure, Stéphanie (S); Rochette, Luc (L); Tomé, Daniel (D); Mariotti, François (F);

Affiliation: AgroParisTech, CRNH-IdF, UMR914 Nutrition Physiology and Ingestive Behavior, F-75005 Paris, France.

Journal and publication information

Publication Type: Journal Article; Research Support, Non-U.S. Gov't

Journal: Nitric oxide : biology and chemistry / official journal of the Nitric Oxide Society (Nitric Oxide), published in United States. (Language: eng)

Reference: 2009-Aug; vol 21 (issue 1) : pp 37-43

Dates: Created 2009/07/14; Completed 2009/10/22;

PMID: 19416758, status: MEDLINE (last retrieved date: 10/22/2009)

Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.

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MeSH headings (categories)

This article was linked to the MeSH Headings (categories) shown below.

Acetylcholine - pharmacology Animals Atrial Natriuretic Factor - blood Biological Availability Biological Markers - blood Cyclic GMP - blood Data Interpretation, Statistical Diet, Atherogenic

Endothelium, Vascular - drug effects; metabolism Male Nitric Oxide - biosynthesis; metabolism Oxidative Stress Postprandial Period - physiology Rats Rats, Inbred WKY Triglycerides - blood

Note: Bold headings indicate primary MeSH headings or qualifiers.

Associated Chemicals: Biological Markers (0) ; Triglycerides (0) ; Nitric Oxide (10102-43-9) ; Acetylcholine (51-84-3) ; Cyclic GMP (7665-99-8) ; Atrial Natriuretic Factor (85637-73-6)

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