V1 receptor signaling is mainly represented by V1aR and V1bR, two arginine vasopressin receptor subtypes that mediate physiological functions beyond renal V2R antidiuresis, including cardiovascular homeostasis, hormone secretion, and social behavior
[1]. Mechanistically, V1aR is originally found in vascular smooth muscle, whereas V1bR is originally found in the anterior pituitary, providing an isoform-level distinction for experimental design
[1]. In disease and behavioral models, male V1aR knockout mice show markedly reduced anxiety-like behavior and profound impairment in social recognition, while V1aR re-expression in the lateral septum rescues social recognition
[2][3]. Compared with OTR, V1bR, and V2R, selective V1aR ligands remain important because receptor and peptide homology can limit subtype-specific interpretation
[4]. For experimental applications,
[D-Arg8]-inotocin acts as a stable competitive V1aR antagonist with 3,000-fold binding selectivity over OTR, V1bR, and V2R
[4].