Abstract: Objective To explore the potential differential metabolites related to blood pressure changes in spontaneously hypertensive rats ( SHR). Methods We applied non-targeted metabolomics technology to study the differences in serum metabolites between SHR and normal groups at 5, 7 and 9 weeks of age, screening out metabolites that co-existed in rats of different ages. We then used SIMCA-P software to analyze the correlation between the metabolomics data and blood pressure and to discover its impact on blood pressure elevation. Finally, we used the MetaboAnalyst platform to conduct a pathway analysis of related metabolites and to identify the related pathways that cause blood pressure changes. Results Through database query, the following 10 differential metabolites that were present at different ages were identified: choline, arachidonic acid, docosahexaenoic acid, thromboxane B2 , uric acid, 16-hydroxyhexadecanoic acid, dodecanedioic acid, cholic acid, 12(13)-DiHOME, and taurochenodeoxycholic acid. At 7 weeks of age, thromboxane B2 was positively correlated with blood pressure, while docosahexaenoic acid, uric acid, dodecanedioic acid, cholic acid, and arachidonic acid were negatively correlated with blood pressure; at 9 weeks, docosahexaenoic acid, dodecanedioic acid and bile acids were positively correlated with blood pressure, while thromboxane B2 , uric acid, and arachidonic acid were negatively correlated with blood pressure. Conclusions The arachidonic acid pathway is the main influencing pathway for the occurrence of hypertension. From overall view, docosahexaenoic acid and bile acids have a certain antihypertensive effect. Uric acid promotes the increase of blood pressure, while the correlation of thromboxane B2 and arachidonic acid with blood pressure is not uniform in the process of blood pressure increase, but they have important effects on the increase of blood pressure.