动物造模,盐敏感性高血压 z-bio 2022-11-16 419

　　Objective: To investigate the role and molecular mechanism of platelets in high-salt-induced salt-sensitive hypertension.

　　Methods: In the in vivo experiment, 25 2-month-old salt-sensitive hypertensive rats (dahl salt-sensitive, Dahl SS) were randomly divided into three groups: low-salt (0.12% NaCl, LS), high-salt (8% NaCl) , HS) and platelet inhibitor (8% NaCl + platelet inhibitor, HS + bus) for 6 weeks. The arterial blood pressure of rats was detected by tail-cuff method, and the platelet activation rate, Ca2+ concentration in platelets, platelet-leukocyte aggregation (PLA) and the proportion of immune cells in aortic vessels were analyzed by flow cytometry. Expression of serum inflammatory factor IL-6. The platelets of SD rats were isolated in vitro and divided into normal salt group (0.9%NaCl) and high salt group (1.3%NaCl), and the differences in Ca2+ concentration and p-selectin expression in platelets were detected.

　　Results: Compared with the low-salt group, the high-salt-fed Dahl SS rats had significantly higher arterial blood pressure, peripheral blood platelet activation rate, platelet-leukocyte aggregation ratio, and aortic vascular immune cell ratio significantly increased, and serum inflammatory factor IL The level of -6 was significantly increased; platelet inhibitors can significantly reduce the increase of blood pressure caused by high salt, inhibit platelet activation, reduce the proportion of peripheral blood PLA and aortic vascular immune cells, and reduce the release of peripheral blood inflammatory factor IL-6; After the rat platelets isolated and purified in vitro were treated with high salt, the concentration of Ca2+ in the platelets increased, and the expression of p-selectin on the platelet surface increased (P < 0.05).

　　Conclusion: High salt activates vascular inflammation by activating platelets and participates in the pathological process of salt-sensitive hypertension, and the mechanism may be related to the increase of Ca2+ concentration in platelets induced by high salt. However, how high salt leads to platelet activation and the specific mechanism of how platelet activation leads to the occurrence and development of hypertension through inflammatory response need further study.