Receptor for apelin receptor early endogenous ligand (APELA) and apelin (APLN) hormones coupled to G proteins that inhibit adenylate cyclase activity. Plays a key role in early development such as gastrulation, blood vessels formation and heart morphogenesis by acting as a receptor for APELA hormone (PubMed:28854362, PubMed:28890073, PubMed:28663440). May promote angioblast migration toward the embryonic midline, i.e. the position of the future vessel formation, during vasculogenesis (By similarity). Promotes sinus venosus (SV)-derived endothelial cells migration into the developing heart to promote coronary blood vessel development (PubMed:28890073). Also plays a role in various processes in adults such as regulation of blood vessel formation, blood pressure, heart contractility and heart failure (PubMed:28371822). After exposure to apelin (APLN) or apelin receptor early endogenous ligand (APELA), internalized from the cell surface into an endosomal recycling compartment, from where it is recycled to the cell membrane. Expressed in coronary endothelial cells (at protein level) (PubMed:28890073). Expressed in the embryo, allantoic and endothelial precursor cells of the yolk sac at 8 days post-coitum (dpc) (PubMed:28663440). Expressed in the secondary heart field and somite at 8.25 dpc (PubMed:28854362). Expressed in fetal allantoic endothelial cells at 9 dpc (PubMed:28663440). Expressed in the allantoid and the invading fetal vasculature of the placenta at 9.5 dpc (PubMed:28854362). Expressed in endothelial cells adjacent to syncytiotrophoblast cells at 10.5 dpc (PubMed:28663440). Expressed weakly in the embryonic heart at 11.5 dpc (PubMed:26611206). Expressed in the adult heart (PubMed:26611206). Expressed in endothelial cells and cardiomyocytes and weakly expressed in fibroblasts (PubMed:10473142, PubMed:26611206). Expressed from embryonic 8 days post-coitum (dpc) throughout the subsequent stages of formation of the cardiovascular system (PubMed:10473142). Up-regulated following myocardial infarction (MI) (at protein level) (PubMed:26611206). Mice lacking APLNR are not represented at Mendelian ratios. Mutant embryos exhibit incomplete penetrance of embryonic lethality (PubMed:28854362, PubMed:28663440). Mutant embryos display improper establishment of the fetal-maternal circulation, such as underdeveloped yolk sac vasculature, embryonic vascular malformations and impaired cardiac tube looping at 10.5 dpc (PubMed:28854362, PubMed:28663440). Mice heart of embryos show reduced coronary vessel growth at 13.5 dpc (PubMed:28890073). The heart of mutant adult mice induced by pressure overload display no improvement in cardiac dysfunction, hypertrophy and fibrosis in response to peptide hormone APELA treatment (PubMed:28371822). Conditional knockout in heart endothelial cells leads to delayed progression of vessel growth onto the heart and reduced branching of the developing coronary plexus in both the subepicardial and intramyocardial layers at 13.5 and 15.5 dpc (PubMed:28890073). Conditional endothelial-specific knockout adult mice, despite severe embryonic coronary vessel defects recover normal cardiac functions; endocardial-derived coronary vessels expand to rescue defective sinus venosus development in a APELA-APLNR-independent manner (PubMed:28890073). Double knockout mice of APLNR and APELA genes exhibited the same penetrance and embryonic lethality as single APELA knockout mice (PubMed:28854362). Belongs to the G-protein coupled receptor 1 family.