动物实验,盐敏感性高血压 z-bo 2020-09-02 399

　　Objective: To explore the role of platelets in salt-sensitive hypertension caused by high salt and its molecular mechanism.

　　Method: In an in vivo experiment, 25-month-old salt-sensitive hypertensive rats (Dahlsalt sensitivity, DahlSS) were randomly divided into three groups: low salt (0.12% NaCl, LS) and high salt. (8% NaCl), HS) and platelet inhibitor (8% NaCl + platelet inhibitor, HS + bath) for 6 weeks. The tail-cuff method was used to detect the arterial blood pressure in rats, and the flow cytometry was used to detect the platelet activation rate, platelet Ca2 + concentration, platelet leukocyte aggregation (PLA) and the percentage of immune cells in the aortic vessels. Analyze the expression of inflammatory factor IL-6 and use ELISA method to detect serum. We isolated platelets from SD rats and divided them into normal salt group (0.9% NaCl) and high salt group (1.3% NaCl) for in vitro experiments to determine the difference in Ca2 + concentration and platelet p-selectin expression . detected.

　　Result: The arterial blood pressure of DahlSS rats fed with high salt was significantly increased, and the platelet activation rate of peripheral blood, platelet white blood cell aggregation rate and aortic vascular immune cell rate were all higher than those of the low salt group. The level of serum inflammatory factor IL-6 is greatly increased. Platelet inhibitors can significantly inhibit the increase in blood pressure caused by high salt, inhibit platelet activation, reduce the ratio of PLA in peripheral blood to aortic immune cells, and release the peripheral blood inflammatory factor IL-6, which can be isolated in vitro with high salt concentration for suppression After the purified rat platelets were treated, the Ca2 + concentration in the platelets increased, and the expression of p-selectin on the platelet surface increased (P\u003c0.05).

　　Conclusion: High salinity participates in the pathological process of salt-sensitive hypertension by activating platelets and vascular inflammation. This mechanism may be related to the increase in platelet Ca2 + concentration caused by high salinity. However, the specific mechanism of how high salinity causes platelet activation and leads to the development and development of hypertension through inflammatory response needs further research.