Changes in cardiovascular responses to chemoreflex activation of rats recovered from protein restriction are not related to AT1 receptors.

Abstract

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 (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 (20mg 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 CG105 animals (332±22 beatsmin−1 and 856±112 ml kg−1 min−1).Mean arterial pressure was not different between the groups.Pressor andbradycardic responses evokedbyKCN(60μgkg−1) were increased in R-PR (+45±13mmHgand−77±47 beatsmin−1) comparedwithCG105 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 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.