In ageing aorta endothelial cells, Valsartan is a synthetic antagonist of non-peptide angiotensin II type 1 receptor that dilates blood vessels and reduces blood pressure by blocking the action of angiotensin. Valsartan significantly decreases the expression of AT1R [1].The pretreatment of valsartan can inhibit TLR2 signaling and proinflammatory cytokines. The expression of AGTR1 was up-regulated after alcohol exposure and was blocked by valsartan pretreatment[2].

In rats after MI. Heart function, Valsartan significantly attenuates the expression of TGF-β/Smad, Hif-1α and fibrosis-related protein , infarcted size, wall thickness as well as myocardial vascularization of ischaemic hearts are also significantly improved by valsartan compared with saline and hydralazine[3]. Valsartan partially reverses the effects of high-salt diet on hypertension, cardiac injuries such as fibrosis and inflammatory cell infiltration, and inhibition of aquaporin 1 and angiogenic factors; valsartan alone does not exert such effects[4]. Valsartan is an effective antidepressant/antianxiety reagent and can promote the hippocampal neurogenesis and expression of BDNF.Long-term use of valsartan (5-40 mg/kg/d, oral) increases the time spent in OFT field centers and the latency to eating in NSF, reduces the fixed time of TST and FST, and increases the preference for sucrose SPT[5].