The anterior cingulate cortex (ACC) has recently emerged as a cortical structure involved in fluid homeostasis. Extracellular dehydration increases the synthesis of angiotensin II, which acts on receptors in the brain to mediate fluid ingestion. This study investigated the role of angiotensin receptor-containing neurons within the ACC in the regulation of fluid homeostasis. We found an abundance of neurons within the ACC that express angiotensin type 2 receptors (referred to as ACC^AT2R). To determine whether ACC^AT2R are thirst sensitive, we delivered Cre-inducible adeno-associated virus synthesizing the calcium indicator, GCaMP6f, into the ACC of male AT₂R-Cre mice. Following implantation of a GRIN lens targeting the ACC, we used a head-mounted miniscope to record calcium events in conscious freely-moving mice. Dehydration excited a subset of ACC^AT2R but these neurons became inhibited upon rehydration with water ingestion. RNAscope in situ hybridization revealed that ACC^AT2R neurons are either GABAergic or glutamatergic. Follow-up anatomical and electrophysiological studies confirmed that GABAergic ACC^AT2R are inhibitory inter-neurons that make inhibitory synapses onto neighboring neurons, whereas glutamatergic ACC^AT2R form functional glutamatergic projections to thalamic nuclei. Next, we utilized intersectional genetics to selectively target GABAergic ACC^AT2R and reveal that optogenetically exciting this subset of neurons attenuates dehydration-induced water intake. Conversely, optogenetically exciting the subset of ACC^AT2R fibers that project to the thalamus increases water intake. The collective implication of the studies is that the excitatory/inhibitor balance of ACC^AT2R modulates the sensation of thirst by mediating fluid homeostasis.