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High salt intake reduces nitric oxide‐dependent control of arteriolar tone in the mouse
Author(s) -
Nurkiewicz Timothy R.,
Boegehold Matthew A.
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.5.a1150
Subject(s) - nitric oxide , medicine , endocrinology , sodium nitroprusside , chemistry , vasodilation , arteriole , acetylcholine , nitric oxide synthase , microcirculation , skeletal muscle , endothelium
We have consistently found that in skeletal muscle arterioles of normotensive rats fed a high salt diet, the bioavailability of endothelium‐derived nitric oxide (NO) is reduced by the activity of reactive oxygen species. Because the impact of dietary salt on resistance vessel function has not been well studied in other species, we investigated arteriolar responses to endothelium‐dependent and ‐independent agonists in the spinotrapezius muscle of C57BL/6J mice fed normal (0.45%, NS) or high salt (7%, HS) diets for 4 weeks. Mean arterial pressure in HS mice was not different from that in NS mice. Arteriolar inner diameters (38±1 μm) were also not different between groups, but the magnitude of arteriolar dilation in response to different concentrations of acetylcholine (ACh) was 50–70% smaller in HS mice than in NS mice. In NS mice, inhibition of nitric oxide synthase with N G monomethyl L‐arginine (L‐NMMA) significantly reduced resting diameters (by 12±4%), and reduced responses to ACh by 46–64%. In contrast, L‐NMMA had no effect on resting arteriolar diameters or responses to ACh in HS mice. Vascular smooth muscle responsiveness to NO, as assessed by arteriolar responses to sodium nitroprusside, was identical in HS and NS mice. These findings suggest that high salt intake, in the absence of hypertension, leads to diminished microvascular NO levels in skeletal muscle of the mouse. (Support: NIH 44012, HEI 4730)