Thank you for visiting nature. You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser or turn off compatibility mode in Internet Explorer. In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript. In this study, we investigated some mechanisms involved in sodium-dependent hypertension of rats exposed to chronic salt NaCl intake from weaning until adult age.
Weaned male Wistar rats were placed under high 0. Water consumption, urine output and sodium excretion were higher in HS rats compared to control.
Blood pressure BP was directly measured by the arterial catheter and found Heart rate variability analysis revealed sympathetic prevalence on modulation of the systolic interval. HS diet did not affect creatinine clearance. Kidney histological analysis revealed no significant change in renal corpuscle structure. Sodium and potassium concentrations in CSF were found higher in HS rats despite no change in plasma concentration of these ions.
Sodium is an essential nutrient and the primary cation in the extracellular fluid. It is required in a number of physiologic processes as maintenance of extracellular volume and osmolality, membrane potentials and several transmembrane transport processes. High salt intake has been associated with high blood pressure BP since , when Ambard and Beaujard first established this correlation 4.
Since then, an overwhelming number of studies have been made on this topic and linked hypertension to high-sodium intake both in humans 3 and experimental 5 , 6 , 7 , 8 , 9 , 10 , 11 , 12 models. Yet, some questions regarding salt-dependent hypertension remain elusive, in particular, those concerning whether the amount of daily sodium consumption in the diet by humans can, per se , elicit hypertension in rodent models.
