Abstract Fri039: Sympathetic-associated macrophage populations are altered in superior cervical ganglia of hypertensive rats

Hypertension (HT) is a global health burden, requiring more effective treatments. Sympathetic activity from the superior cervical ganglia (SCG) modulates cardiac function, and sympathetic hyperactivity is associated with HT. However, the mechanisms underlying this outcome are poorly understood. Recent studies have suggested that macrophages (MPs) residing in the sympathetic ganglia may regulate the activity of cardiac sympathetic neurons. For example, co-culturing MPs from a hypertensive rat with normotensive sympathetic neurons potentiates neuronal activity. Studies have shown that depletion of MPs from the SCG can restore normal sympathetic neuronal activity. These findings suggest that disruptions of the crosstalk between the nervous and immune systems in peripheral sympathetic ganglia could influence cardiovascular disease progression. Furthermore, changes in MP morphology are reported to reflect their activation status, i.e. a change from a complex, branched morphology to a spherical less complex morphology. Therefore, this study aimed to examine changes in MP populations and morphology in the SCG from normotensive (Wistar Kyoto; WKY) and hypertensive (SHR) rats. SCGs from age-matched WKY and SHR rats were labeled with antibodies targeting IBA1 (Ionized Ca2+ binding adapter molecule-1; MP marker) and βIII-tubulin (neuronal marker) to create 3D images from confocal Z-stacks. The number and morphology of MPs and their interactions with neurons were examined. In SCG taken from the 20-week-old WKY and SHR groups, the number of IBA1+ MPs was higher in the SHR group compared to WKY. Morphologically, the level and complexity of branching of MPs decreased in SHR vs WKY SCG. These effects were accentuated when comparing 30-week-old SHR with 20-week-old animals. These data suggest that MPs may contribute to the development of sympathetic neuronal pathology in HT. Changes in MP morphology, i.e., decreased branching, suggest a change to an active MP phenotype during HT. Future studies include determining whether the increased number and activation state of MPs contribute to sympathetic hyperactivity and investigating specific inflammatory signaling pathways as potential therapeutic targets for HT treatment.