Objective: To establish a salt-sensitive hypertensive mouse model and use the antihypertensive drug nifedipine to verify the model.
Method: C57BL/6J mice were studied, and a normal group fed with a regular diet, a high-salt group fed with a high-salt diet, and a high-salt diet intervention group fed with 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 determine 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 mice in the high-salt group were significantly higher than those of the normal group (all P≥0.01), but the blood pressure of the intervention group mice was significantly increased (all P≥0.01). u003c0.01). Compared with the normal group, the liver function indexes of the mice in the high salt group were aspartate aminotransferase, alkaline phosphatase, albumin, serum total protein and direct bilirubin levels, blood lipid indexes cholesterol, and kidney function indexes were all uric acid And calcium. The intervention group gradually recovered, and the ion and magnesium ion levels changed significantly (both P\u003c0.05). Histopathology showed that the liver and kidney of the mice in the high-salt group had varying degrees of damage.
Conclusion: High-salt diet has successfully established a salt-sensitive hypertensive mouse model, and nifedipine can effectively reduce the blood pressure of the model mice.