Microvascular changes associated with high salt intake and hypertension in Dahl rats.
This study was undertaken to determine if an active reduction in small arteriole diameters or functional closure of these vessels contributes to increased vascular resistance in inbred hypertensive Dahl salt-sensitive (SS/Jr) rats. Fluorescence microscopy was used to study the spinotrapezius muscle arteriolar network in SS/Jr fed high (7%) or low (0.45%) salt diets for 4 weeks. Dahl salt-resistant (SR/Jr) rats fed high or low salt diets were also studied to evaluate the exclusive effect of dietary salt on the microvasculature. High salt intake did not alter arterial pressure in SR/Jr, but caused marked hypertension (mean arterial pressure = 168 mm Hg) in SS/Jr. The diameter of large (arcade bridge) arterioles was significantly smaller in SS/Jr than SR/Jr, regardless of diet. The establishment of hypertension in SS/Jr was accompanied by an active diameter reduction in the intermediate (arcade) arterioles. However, there were no differences among groups in the density of perfused small arterioles or their diameters, and arteriolar density did not change with abolition of vascular tone in any group. In both strains, high salt intake reduced the passive diameter of large arterioles by 20%. Therefore, the establishment of hypertension in SS/Jr rats is associated with increased tone of proximal, but not distal, arterioles. In addition, distal arteriole rarefaction (functional or structural) does not contribute to increased spinotrapezius muscle resistance at this stage of salt-induced hypertension. The salt-induced reduction in passive arteriolar diameters suggests that high salt intake alone can alter the structural and/or mechanical properties of the arteriolar wall.