Abstract Hypertension (HTN), when prolonged, extends beyond the cardiovascular system, impairs neurovascular function, and progresses into cognitive impairment. Thus, it is essential to understand the mechanism that drives HTN-induced brain pathogenesis for devising novel therapy. This study explored spatial learning, vessels-associated microglia and neuroinflammation during angiotensin II (Ang II) induced HTN with the hypothesis that after HTN induction, endogenous H 2 S level contributes to ne
