OBJECTIVE: To investigate the potential mecha-nism of the vascular remodeling effect and provide additional information about anti-hypertension ac-tivity of Fufang Qima capsule (e-m(sic)QM). METHODS: Spontaneous hypertensive rats (SHRs) were used to study the underlying mechanism of the anti-hypertension activity of QM. In this study, SHRs were randomly divided into 5 groups: model group, Telmisartan group (7.2 mg/kg, p.o.), and three QM groups (0.9298, 1.8596, and 3.7192 g/kg, p.o.). Wistar Kyoto rats (WKY) were used as normal control group. Blood pressure (BP), aorta, perivascu-lar adipose tissue (PVAT) histology were investigat-ed to evaluate the effect of QM. Nitric oxide (NO) and endothelial nitric oxide synthase (eNOS) phos-phorylation were measured. Adiponectin (APN) se-cretion, as well as APN signal pathway proteins in-cluding APN, adiponectin receptors (R1 and R2) and adenosine 5'-monophosphate-activated pro-tein kinase (AMPK) were all analyzed. RESULTS: QM significantly reduced BP and amelio-rated the vascular pathological change, i.e. intima media thicken and collagen fiber hyperplasia. Meanwhile, QM increased concentration of NO and the phosphorylation of eNOS in the aorta. The an-ti-hypertensive and endothelia-protective effect of QM could be attributed to activating APN/ AMPK pathway by up-regulating the expression of APN in PVAT and APN Receptor 2, AMPK alpha and phosphory-lated AMPK alpha in the aorta. CONCLUSION: The QM alleviation effect mecha- nism for primary hypertension was via modulating the APN/AMPK signal pathway. (c) 2021 JTCM. All rights reserved.