Emerging roles of astrocytes in autonomic control of blood pressure and hypertension.

Astrocytes, traditionally viewed as passive support cells, have emerged as critical regulators of neuronal signaling, autonomic function, and cardiovascular homeostasis. Accumulating evidence highlights the active participation of astrocytes in maintaining neurotransmitter balance, ion homeostasis, synaptic plasticity, and cerebral metabolism. In particular, astrocytes form integral components of tripartite synapses, mediating neuronal communication through calcium-dependent release of gliotransmitters, including ATP, glutamate, d-serine, and γ-aminobutyric acid. This astrocyte-mediated signaling is essential in modulating autonomic circuits involved in blood pressure regulation and sympathetic nerve activity. Recent research underscores the role of astrocyte dysfunction-mediated inflammation, termed astrogliosis, in driving pathological states such as hypertension. Astrocyte activation within critical cardiovascular control centers, including the nucleus tractus solitarii, paraventricular nucleus, and rostral ventrolateral medulla, promotes neuroinflammation, disrupts neurotransmitter clearance, and enhances sympathetic nervous system activity. These processes contribute significantly to hypertension development, particularly under conditions of metabolic stress, such as obesity and high-fat diet consumption. Key molecular mechanisms implicated include NF-κB-mediated inflammatory pathways, impaired astrocytic glutamate transporters, overactivation of angiotensin II signaling, and abnormal gliotransmitter release. In this review, we summarize recent advances in our understanding of the physiological roles of astrocytes in autonomic and cardiovascular regulation and discuss the pathological consequences of astrocyte-driven neuroinflammation in hypertension. We further outline promising directions for future research and therapeutic interventions targeting astrocytic pathways, offering potential new strategies for preventing or reversing autonomic dysfunction and hypertension.