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 (0.90% w/w, HS) or regular (0.27% w/w, Cont) sodium diets for 12 weeks. 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 13.8% higher in HS vs Cont rats. Ganglionic blockade with hexamethonium caused greater fall in the BP of HS rats (33%), and central antagonism of AT1 receptors (losartan) microinjected into the lateral ventricle reduced BP level of HS, but not of Cont group. 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. Taken together, data suggest that animals exposed to chronic salt intake to a level close to that reported for human’ diet since weaning lead to hypertension, which appears to rely on sodium-driven neurogenic mechanisms.

Edited by: Jian Wang New Findings r What is the central question of this study?In this study, we sought to investigate whether cardiovascular responses to peripheral chemoreflex activation of rats recovered from protein restriction are related to activation of AT 1 receptors. r What is the main finding and its importance?This study highlights the fact that angiotensinergic mechanisms activated by AT 1 receptors do not support increased responses to peripheral chemoreflex activation by KCN in rats recovered from protein restriction. Also, we found that protein restriction led to increased resting ventilation in adult rats, even after recovery.The effects of a low-protein diet followed by recovery on cardiorespiratory responses to peripheral chemoreflex activation were tested before and after systemic angiotensin II type 1 (AT 1 ) receptor antagonism. Male Fischer rats were divided into control and recovered (R-PR) groups after weaning. The R-PR rats were fed a low-protein (8%) diet for 35 days and recovered with a normal protein (20%) diet for 70 days. Control rats received a normal protein diet for 105 days (CG 105 ). After cannulation surgery, mean arterial pressure, heart rate, respiratory frequency, tidal volume and minute ventilation were acquired using a digital recording system in freely moving rats. The role of angintensin II was evaluated by systemic antagonism of AT 1 receptors with losartan (20 mg kg −1 i.v.). The peripheral chemoreflex was elicited by increasing doses of KCN (20-160 μg kg min −1 , i.v.). At baseline, R-PR rats presented increased heart rate and minute ventilation (372 ± 34 beats min −1 and 1.274 ± 377 ml kg −1 min −1 ) compared with CG 105 animals (332 ± 22 beats min −1 and 856 ± 112 ml kg −1 min −1 ). Mean arterial pressure was not different between the groups. Pressor and bradycardic responses evoked by KCN (60 μg kg −1 ) were increased in R-PR (+45 ± 13 mmHg and −77 ± 47 beats min −1 ) compared with CG 105 rats (+25 ± 17 mmHg and −27 ± 28 beats min −1 ), but no difference was found in the tachypnoeic response. These differences were preserved after losartan. The data suggest that angiotensin II acting on AT 1 receptors may not be associated with the increased heart rate, increased minute