动物造模,盐敏感性高血压 z-bio 2022-09-30 455

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

　　Methods: 2-month-old salt-sensitive rats (DahlSS) and control salt-tolerant rats (SS-13BN) were given low salt (0.12%NaCl, LS), high salt (8%NaCl, HS), high salt, respectively. The rats were fed with salt and aspirin by gavage ((10 mg/(kg·d)), HS+ASA) for 8 weeks. During this period, the arterial blood pressure was continuously measured by tail cuff method. After 8 weeks, the arterial blood pressure of the rats was measured by intubation of the common carotid artery. The expression of inflammatory factors IL-6, IL-1β and TNF-α in renal tissue was detected by timePCR, the number of skin M2 macrophages was detected by immunofluorescence, and the expression of vascular function representative proteins eNOS and vWF was detected by western blot.

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

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