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Maternal High‐Sucrose Diet Accelerates Vascular Stiffness in Aged Offspring via Suppressing Ca v 1.2 and Contractile Phenotype of Vascular Smooth Muscle Cells
Author(s) -
Feng Xueqin,
Li Xiang,
Yang Chunli,
Ren Qinggui,
Zhang Wenna,
Li Na,
Zhang Meng,
Zhang Bo,
Zhang Lubo,
Zhou Xiuwen,
Xu Zhice
Publication year - 2019
Publication title -
molecular nutrition and food research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.495
H-Index - 131
eISSN - 1613-4133
pISSN - 1613-4125
DOI - 10.1002/mnfr.201900022
Subject(s) - offspring , endocrinology , mesenteric arteries , medicine , vascular smooth muscle , insulin resistance , phenylephrine , arterial stiffness , fetus , insulin , biology , pregnancy , blood pressure , artery , genetics , smooth muscle
Scope The fetal programming in response to over‐nutrition during pregnancy is involved in pathogenesis of cardiovascular diseases later in life. The authors’ previous work reported that prenatal high‐sucrose (HS) diet impaired functions of large‐conductance Ca 2+ ‐activated K + channels (BK) in mesenteric arteries in the adolescent offspring rats. This study determines whether prenatal HS has a long‐term impact on resistance vasculature in the aged offspring rats. Methods and results Pregnant rats are fed with a high‐sucrose diet until delivery. Aged offspring from prenatal HS exhibit elevated fasting insulin level, insulin resistance index, and diastolic pressure. Both pressure‐induced myogenic responses and phenylephrine‐stimulated contraction of mesenteric arteries in HS are weakened. Electrophysiological tests and western blot indicate that BK and L‐type calcium channels (Ca v 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 α‐smooth muscle actin is decreased, and insulin/insulin receptor/phosphoinositide3‐kinase (PI3K) signaling pathway is downregulated. Conclusion The results suggest that prenatal HS induced stiffness of mesenteric arteries in aged offspring by inhibiting Ca v 1.2 function and PI3K‐associated contractile phenotype of VSMCs.