Objective: To establish a salt-sensitive hypertensive mouse model and verify the model with the antihypertensive drug nifedipine.
Method: C57BL/6J mice were studied, and the normal diet group, high-salt diet group, high-salt diet group and high-salt diet intervention group, nifedipine were set up. A non-invasive blood pressure measurement system was used to measure the blood pressure changes of each group of mice. The blood biochemical analyzer is used to measure liver function, kidney function, blood lipids, blood sugar, ions and other biochemical indicators. Mouse serum; hematoxylin-eosin staining is used to observe small histological changes in rat liver, kidney and carotid artery.
Results: The systolic and diastolic blood pressures of the high-salt group mice were significantly higher than those of the normal group (all P \u003cu003c0.01), but the blood pressure of the intervention group mice was significantly higher. All P\u003c0.01). Compared with the normal group, the liver function indexes of the mice in the high salt group included aspartate aminotransferase, alkaline phosphatase, albumin, total serum protein and direct bilirubin levels, blood lipid indexes cholesterol, renal function indexes uric acid and calcium . The intervention group gradually recovered, and the magnesium ion level changed significantly (all P\u003cP0.05). Histopathology showed that the liver and kidney of the mice in the high salt group had varying degrees of damage.
Conclusion: A high-salt diet can successfully establish a salt-sensitive hypertensive mouse model, and nifedipine can effectively reduce the blood pressure of the model mice.