Chronic elevations in salt intake and reduced renal mass hypertension compromise mechanisms of arteriolar dilation.

Alterations in the reactivity of arterioles to vasodilator agonists were assessed in the skeletal muscle microcirculation of age-matched, normotensive male Sprague-Dawley rats fed either a high salt (4% NaCl, HS) or a low salt (0.4% NaCl, LS) diet and in reduced renal mass hypertensive rats on a high salt diet (HSRRM) for 4 weeks. The in situ superfused cremaster muscle was prepared for observation by television microscopy. Changes in the microvessel diameter in response to acetylcholine, iloprost, cholera toxin, forskolin, or sodium nitroprusside were measured with a video micrometer. Arteriolar responses to each of the agonists were decreased under both HS and HSRRM conditions. Maximum arteriolar diameter (determined during superfusion with Ca2+-free solution containing 10(-4) M adenosine) was reduced in HS and HSRRM rats, suggesting anatomic remodeling of the vessels. In normotensive animals on the HS diet, the decreased reactivity was in proportion to the remodeling so the sensitivity index (vascular reactivity corrected for the anatomic remodeling) was not altered. Vascular responses in HSRRM rats were depressed to an extent disproportionate to the remodeling, so that the sensitivity index to the vasodilator agonists was significantly reduced. We conclude that HSRRM hypertension and HS diet (independent of hypertension) can have significant effects on the structure of microvessels and on the reactivity of the arterioles to dilator agonists. The severity of these alterations is greater in HSRRM hypertension than in normotensive rats on HS diets.