The hypothesis that long-term administration of a physiologically relevant high salt diet to rats leads to the development of structural vascular changes that predispose to hypertension was tested. Adult male Sprague-Dawley rats were fed 2% NaCl diet for 3 or 6 months; rats fed 0.7% NaCl diet were controls. Then, the systemic circulation of the rats was perfusion-fixed at 100 mm Hg. The junction of the mesentery and small intestine, the renal cortex, and segments of left carotid artery, thoracic aorta, and second order mesenteric arteries were embedded in paraffin or epoxy for morphometric measurements. The average monthly tail systolic blood pressure (BP) of salt-fed rats at 3 and 6 months were unchanged. The following morphometric changes in salt-fed rats were observed: 1) dilatation of the carotid artery at 3 months (P <.05); 2) dilatation and reduced wall-to-lumen ratio of the second order mesenteric artery (P <.01); 3) increased wall-to-lumen ratio of small mesenteric resistance arteries (P <.01); 4) reduced wall-to-lumen ratio of renal cortical resistance arteries at 6 months (P <. 05); and 5) unchanged structure of aorta. The long-term administration of a high salt diet leads to structural vascular changes in normotensive rats. There are important regional and segmental variations in the long-term adaptation of arteries to a high salt diet.

Geometry (increased or unchanged lumen and increased wall thickness), rather than increased stiffness of wall components, appears to be the cause of reduced distensibility of arteries in DS rats. Structural and functional adaptation to salt sensitivity may occur on what is considered a 'normal' sodium diet.

A three-fold increase in dietary sodium intake leads to dilatation of arteries in normotensive rats. When there is compensatory remodeling, the distensibility of arteries remains unchanged; when compensation is lacking, unopposed dilatation is associated with reduced distensibility.

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