盐敏感性高血压,阿司匹林 z-bo 2020-11-21 341

　　Objective: To explore the regulatory effect and related mechanisms of aspirin on salt-sensitive hypertension in rats.

　　Methods: 2-month-old salt-sensitive rats (DahlSS) and their control salt-tolerant rats (SS-13BN) were given low salt (0.12% NaCl, LS), high salt (8% NaCl, HS), and high salt. Gavage with salt and aspirin ((10mg/(kg d)), HS+ASA) for up to 8 weeks, during which the arterial blood pressure was continuously measured by the tail cuff method. After 8 weeks, the common carotid artery was intubated to measure the arterial blood pressure of the rat, Real- TimePCR was used to detect the expression of inflammatory factors IL-6, IL-1β, and TNF-α in kidney tissue, immunofluorescence was used to detect the number of skin M2 macrophages, and western blot was used to detect the expression of eNOS and vWF, a representative protein of vascular function.

　　Results: After high salt feeding in DahlSS rats, blood pressure increased significantly, renal tissue inflammatory factors and vascular vWF factor expression increased significantly, the number of skin M2 macrophages and vascular eNOS expression decreased significantly, aspirin can effectively improve DahlSS rats High salt-induced increase in blood pressure, inflammatory response and vascular function damage, but SS-13BN rats did not have the above situation.

　　Conclusion: Aspirin inhibits the inflammatory response induced by high salt in DahlSS rats through antiplatelet function, and inhibits the damage of blood vessel function and the development of hypertension.