Placental endothelial dysfunction represents a unifying pathophysiological interface in gestational diabetes mellitus (GDM) and pre-eclampsia (PE), linking abnormal placentation with metabolic stress and impaired foetoplacental vascular regulation. In GDM, maternal hyperglycaemia, insulin resistance, and inflammation reprogramme the endothelial phenotype by disrupting vasomotor homeostasis and remodelling the adenosine/L-arginine/nitric oxide (ALANO) axis. This disturbance is closely associated with impaired equilibrative nucleoside transporter-dependent adenosine transport, intracellular alkalinization, oxidative stress, and downstream cytoskeletal and epigenetic changes that together compromise placental angiogenesis, barrier integrity, and endothelial signalling. In PE, defective trophoblast invasion and incomplete spiral artery remodelling give rise to placental hypoxia and ischaemia, favouring the release of anti-angiogenic mediators. The resulting loss of NO bioavailability and endothelial repair capacity is amplified by inflammatory and vasoactive signalling, establishing a vasoconstrictor, pro-oxidant, and pro-inflammatory vascular environment. GDM and PE arise from distinct initiating insults, but they meet at the level of endothelial injury through interrelated disturbances in redox balance, inflammatory tone, angiogenic control, and NO-dependent regulation. When both disorders coexist, these derangements are likely to interact in ways that intensify placental hypoperfusion, endothelial dysfunction, and adverse maternal and foetal outcomes. An integrated mechanistic outline centred on endothelial signalling and vascular adaptation may provide stronger basis for biological stratification, biomarker development, and precision therapeutic targeting.