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Abstract: PUB417

Impact of Renal Macrophages on Blood Pressure Regulation via the Neuroimmune System

Session Information

Category: Hypertension and CVD

  • 1601 Hypertension and CVD: Basic

Authors

  • Washimine, Norito, Nagasaki Daigaku Daigakuin Ishiyakugaku Sogo Kenkyuka, Nagasaki, Nagasaki, Japan
  • Umene, Ryusuke, Nagasaki Daigaku Daigakuin Ishiyakugaku Sogo Kenkyuka, Nagasaki, Nagasaki, Japan
  • Wu, Chia-Hsien, Nagasaki Daigaku Daigakuin Ishiyakugaku Sogo Kenkyuka, Nagasaki, Nagasaki, Japan
  • Nakamura, Yasuna, Nagasaki Daigaku Daigakuin Ishiyakugaku Sogo Kenkyuka, Nagasaki, Nagasaki, Japan
  • Matsuo, Sayumi, Nagasaki Daigaku Daigakuin Ishiyakugaku Sogo Kenkyuka, Nagasaki, Nagasaki, Japan
  • Nishino, Tomoya, Nagasaki Daigaku Daigakuin Ishiyakugaku Sogo Kenkyuka, Nagasaki, Nagasaki, Japan
  • Inoue, Tsuyoshi, Nagasaki Daigaku Daigakuin Ishiyakugaku Sogo Kenkyuka, Nagasaki, Nagasaki, Japan
Background

Hypertension affects over a billion people globally and is a risk factor for many diseases. Research shows that macrophages infiltrate various organs and regulate blood pressure. Previous studies noted increased macrophages and phenotype changes in hypertension, but the specific role of kidney macrophage infiltration remains unclear. Additionally, the nervous system influences immune cell dynamics through their neurotransmitter receptors, suggesting a neuro-immune interaction in blood pressure regulation. The precise mechanisms and their connection to the kidney remain unclear. This study aims to explore renal macrophage dynamics in hypertension development and the effects of different neural stimuli on macrophage function.

Methods

Hypertension was induced in mice using subcutaneous angiotensin II administration and oral saline intake. Immune cell subsets in the spleen and kidney were analyzed via flow cytometry. Hypertensive mice lacking macrophages or specific macrophage receptors were also created to assess blood pressure and immune cell changes. The effects of salt loading and pharmacological autonomic stimulation under angiotensin II administration on hypertension development were evaluated. A comprehensive genetic analysis of renal macrophages from hypertensive mice was conducted to identify factors related to hypertension suppression.

Results

The hypertensive group showed an increased number of renal macrophages compared to the control group. Hypertension was suppressed in mice without macrophages or macrophage-specific autonomic receptors. In angiotensin II-induced hypertensive mice, salt loading and pharmacological autonomic stimulation appeared to contribute to hypertension development. Renal macrophages were successfully isolated from hypertensive mice, and genetic analysis is underway to identify related factors.

Conclusion

Macrophages significantly contribute to hypertension pathogenesis through their kidney accumulation. Autonomic stimulation may regulate blood pressure via macrophages. Identifying factors linked to hypertension development from renal macrophages in hypertensive mice could offer new therapeutic targets for hypertension treatment. Stimulating the autonomic nervous system might help uncover underlying mechanisms.