{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,8,29]],"date-time":"2025-08-29T10:27:21Z","timestamp":1756463241104,"version":"3.41.2"},"reference-count":46,"publisher":"Wiley","issue":"14","license":[{"start":{"date-parts":[[2019,5,17]],"date-time":"2019-05-17T00:00:00Z","timestamp":1558051200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81771592","81030006","81320108006"],"award-info":[{"award-number":["81771592","81030006","81320108006"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Molecular Nutrition Food Res"],"published-print":{"date-parts":[[2019,7]]},"abstract":"<jats:sec><jats:title>Scope<\/jats:title><jats:p>The fetal programming in response to over\u2010nutrition during pregnancy is involved in pathogenesis of cardiovascular diseases later in life. The authors\u2019 previous work reported that prenatal high\u2010sucrose (HS) diet impaired functions of large\u2010conductance Ca<jats:sup>2+<\/jats:sup>\u2010activated K<jats:sup>+<\/jats:sup> channels (BK) in mesenteric arteries in the adolescent offspring rats. This study determines whether prenatal HS has a long\u2010term impact on resistance vasculature in the aged offspring rats.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods and results<\/jats:title><jats:p>Pregnant rats are fed with a high\u2010sucrose diet until delivery. Aged offspring from prenatal HS exhibit elevated fasting insulin level, insulin resistance index, and diastolic pressure. Both pressure\u2010induced myogenic responses and phenylephrine\u2010stimulated contraction of mesenteric arteries in HS are weakened. Electrophysiological tests and western blot indicate that BK and L\u2010type calcium channels (Ca<jats:sub>v<\/jats:sub>1.2) are impaired in HS group. On the other hand, expression of matrix metalloproteinase 2 of mesenteric arteries is reduced in HS group while expression of tissue inhibitors of metalloproteinase is increased, indicating that extra cellular matrix (ECM) is remodeled. Furthermore, expression of \u03b1\u2010smooth muscle actin is decreased, and insulin\/insulin receptor\/phosphoinositide3\u2010kinase (PI3K) signaling pathway is downregulated.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>The results suggest that prenatal HS induced stiffness of mesenteric arteries in aged offspring by inhibiting Ca<jats:sub>v<\/jats:sub>1.2 function and PI3K\u2010associated contractile phenotype of VSMCs.<\/jats:p><\/jats:sec>","DOI":"10.1002\/mnfr.201900022","type":"journal-article","created":{"date-parts":[[2019,5,8]],"date-time":"2019-05-08T21:43:37Z","timestamp":1557351817000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":11,"title":["Maternal High\u2010Sucrose Diet Accelerates Vascular Stiffness in Aged Offspring via Suppressing Ca<sub>v<\/sub>1.2 and Contractile Phenotype of Vascular Smooth Muscle 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