engleski

High dietary salt intake impairs vascular reactivity in both micro- and macrocirculation in young healthy individuals

High dietary salt intake is a risk factor for the development of cardiovascular disease that is independent of its ability to increase arterial blood pressure in young healthy individuals. A key feature of this pressure- independent effect is a reduction in vascular reactivity limited by impaired endothelium- dependent dilation. Most studies in humans have focused on conductance and resistance arteries, but since the earliest changes in various pathological conditions occur in the microcirculation, it is important to evaluate changes in the microcirculation, too. In our studies we have demonstrated that high daily salt intake for only 7 days significantly impaires vascular reactivity in both micro- and macrocirculation. High salt intake reduceds vascular NO bioactivity in large conductance arteries, demonstrated by impaired flow mediated dilation (at least 50% contributed by NO). However, some others vasodilator mediators may be involved in changed vascular reactivity in microcirculation. Our results indicate the possible role of the vasoconstrictor metabolites of cyclooxygenase enzymes, specifically COX-1, in development of impaired endothelial function after acute salt loading in humans. Other study on isolated human microvessels suggests that one of the possible mechanisms through which acute salt loading affects vascular function, beside reduced NO bioactivity, is reduced production and/or bioavailability of COX 1, 2 dependent vasodilators.

high salt intake; vascular reactivity; Laser Doppler Flowmetry; Flow Mediated Dilation

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