Lactate inhibited sodium intake in dehydrated rats

Recent studies have suggested that glial cells, especially astrocytes, are involved in balanced hydromineral modulation. In response to increased extracellular Na+ concentration, astrocytic Nax channels are activated, promoting lactate production and release. Furthermore, previous in vitro studies have suggested that lactate and hypertonic Na + solution activate SFO GABAergic neurons involved in the salt-appetite central pathways. Here, we evaluated the role of lactate in dehydration-induced sodium and water intake. To this end, intracerebroventricular microinjection (icv) of L-lactate or alpha-cyano-4-hydroxycinnamic acid (alpha-CHCA, MCT lactate transporter inhibitor) was performed in rats subjected to 48 h of water deprivation (WD) and 1 h of partial rehydration after 48 h of WD (WD-PR). The rehydration protocol was used to distinguish the mechanisms of thirst and sodium appetite induced by WD. Then, water and sodium (0.3 M NaCl) intake were evaluated for 2 h. Our results showed that central alpha-CHCA induced an increase in sodium preference in WD rats. Furthermore, central lactate increased water intake but reduced sodium intake in WD-PR animals. In contrast, central lactate transporter inhibition did not change water or sodium intake in WD-PR rats. Our results suggest that lactate is involved in inhibitory mechanisms that induce sodium intake avoidance in dehydrated rats.