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However, CNI have adverse effects on blood vessels and renal function, which may be linked to cellular senescence. Valsartan, a common angiotensin II type 1 receptor (AT\n                      <jats:sub>1<\/jats:sub>\n                      R) blocker, exhibits anti\u2010senescence properties. We tested the hypothesis that tacrolimus causes hypertension and microvascular remodeling that involves induction of senescence, and that valsartan is protective.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Microperfusion and wire myography were employed to assess the contractile and dilatory functions of renal afferent arterioles (Af\u2010Art) and mesenteric arteries, respectively. The expression of components of the renin\u2010angiotensin system (RAS) and senescence\u2010associated biomarkers was investigated using qPCR and immunohistochemistry.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Long\u2010term administration of Tac activated the RAS. Tac\u2010induced microvascular remodeling in mesenteric arteries and Af\u2010Art was mitigated by treatment with valsartan. Mice treated with Tac exhibited increased vasoconstriction in response to angiotensin II and reduced dilation to acetylcholine. Both effects were abolished by valsartan. Additionally, senescence\u2010associated biomarkers were upregulated in mesenteric and renal resistance arteries from Tac\u2010treated mice. Co\u2010administration of Tac with valsartan or ABT\u2010263, a senolytic agent, rescued Tac\u2010induced microvascular injury and reduced hypertension (conscious mice, noninvasive tail\u2010cuff system). Treatment with the antihypertensive drug amlodipine normalized blood pressure and downregulated senescence\u2010associated beta\u2010galactosidase in mesenteric arteries.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>These findings suggest that cellular senescence contributes to Tac\u2010induced microvascular injury and hypertension and demonstrate the effectiveness of senolytic treatment for protection. Valsartan could reduce senescence indirectly by lowering blood pressure; a direct anti\u2010senescence effect might also play a role in this context.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/apha.70189","type":"journal-article","created":{"date-parts":[[2026,3,12]],"date-time":"2026-03-12T04:16:39Z","timestamp":1773288999000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":3,"title":["Tacrolimus Induced Hypertension and Vascular Remodeling Includes Mechanisms of Cellular Senescence\u2014The Protective Effect of Valsartan"],"prefix":"10.1111","volume":"242","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-9679-0101","authenticated-orcid":false,"given":"Lingyan","family":"Fei","sequence":"first","affiliation":[{"name":"Department of Nephrology, Center of Kidney and Urology The Seventh Affiliated Hospital, Sun Yat\u2010Sen University  Shenzhen 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