Cerebrovascular dysfunction and neuroinflammation play key roles in the pathophysiology of Alzheimer’s disease (AD). The kinin-kallikrein system involving bradykinin receptor has been proposed at the nexus of beta-amyloid, vascular pathology and inflammation in patients with AD and in animal models. Here, we evaluated the effect of blocking the bradykinin receptors 1 and 2 by treatment with the bradykinin antagonist noscapine on cerebrovascular dysfunction, inflammation and amyloid pathology in a transgenic mouse model of amyloidosis. Transgenic arcAβ mice, and wild-type littermates of 14 months-of-age were either treated with noscapine (3 g/L, acidified drinking water) or received drinking water as control for three months (n = 8-11 per group). Arterial spin labeling magnetic resonance imaging showed alleviated regional hypoperfusion in noscapine-treated arcAb compared to control arcAb mice. Functional magnetic resonance imaging showed mitigated reduced regional cerebral vascular reactivity in noscapine-treated arcAb compared to control arcAb mice.