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Maternal high‐salt diets affected pressor responses and microvasoconstriction via PKC/BK channel signaling pathways in rat offspring
Author(s) -
Bo Le,
Jiang Lin,
Zhou Anwen,
Wu Chonglong,
Li Jiayue,
Gao Qinqin,
Zhang Pengjie,
Lv Juanxiu,
Li Na,
Gu Xiuxia,
Zhu Zhoufeng,
Mao Caiping,
Xu Zhice
Publication year - 2015
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.201400841
Subject(s) - offspring , mesenteric arteries , endocrinology , medicine , phenylephrine , blood pressure , vascular smooth muscle , biology , pregnancy , artery , genetics , smooth muscle
Scope High‐salt (HS) intake is linked to hypertension, and prenatal exposure to maternal HS diets may have long‐term impact on cardiovascular systems. The relationship between HS diets and cardiovascular disease has received extensive attention. This study determined pressor responses and microvessel functions in the adult offspring rats exposed to prenatal HS. Methods and results The offspring of 5‐month old as young adults in rats were used. Blood pressure, vascular tone, intracellular Ca 2+ , and BK channels in mesenteric arteries were measured in the offspring. Phenylephrine (Phe)‐induced pressor responses were significantly higher in the prenatal HS offspring. Vessel tension and intracellular Ca 2+ concentrations associated with Phe‐induced pressor responses were increased in the mesenteric arteries of the HS offspring. PKC α‐ and δ‐isoforms were upregulated in mesenteric arteries of the HS offspring. The enhanced Phe‐mediated vascular activity was linked to the altered PKC‐modulated BK channel functions. Conclusion The results suggested that prenatal exposure to HS altered microvascular activity probably via changes in PKC/BK signaling pathways, which may lead to increased risks of hypertension in the offspring.