Abstract

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 AT1 receptors. What is the main finding and its importance? This study highlights the fact that angiotensinergic mechanisms activated by AT1 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 angiotensinII type1 (AT1 ) 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 (CG105 ). 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 AT1 receptors with losartan (20mgkg-1 i.v.). The peripheral chemoreflex was elicited by increasing doses of KCN (20-160μgkgmin-1 , i.v.). At baseline, R-PR rats presented increased heart rate and minute ventilation (372±34beatsmin-1 and 1.274±377mlkg-1 min-1 ) compared with CG105 animals (332±22beatsmin-1 and 856±112mlkg-1 min-1 ). Mean arterial pressure was not different between the groups. Pressor and bradycardic responses evoked by KCN (60μgkg-1 ) were increased in R-PR (+45±13mmHg and -77±47beatsmin-1 ) compared with CG105 rats (+25±17mmHg and -27±28beatsmin-1 ), but no difference was found in the tachypnoeic response. These differences were preserved after losartan. The data suggest that angiotensinII acting on AT1 receptors may not be associated with the increased heart rate, increased minute ventilation and acute cardiovascular responses to peripheral chemoreflex activation in rats that underwent postweaning protein restriction followed by recovery.

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