Maternal high‐salt diets affected pressor responses and microvasoconstriction via PKC/BK channel signaling pathways in rat offspring

• Published in: Molecular nutrition & food research Vol. 59; no. 6; pp. 1190 - 1199
• Main Authors: 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
• Format: Journal Article
• Language: English
• Published: Germany Wiley-VCH 01.06.2015; Blackwell Publishing Ltd
• Subjects: Animals; blood pressure; Blood Pressure - drug effects; calcium; Calcium - metabolism; Diet; Female; Hypertension; Hypertension - etiology; Hypertension - pathology; Large-conductance Ca2+-activated K+ channels; Large-Conductance Calcium-Activated Potassium Channels - genetics; Large-Conductance Calcium-Activated Potassium Channels - metabolism; long term effects; Male; Maternal Nutritional Physiological Phenomena; mesenteric arteries; Mesenteric Arteries - drug effects; Muscle, Smooth, Vascular - drug effects; Muscle, Smooth, Vascular - metabolism; phenylephrine; Phenylephrine - pharmacology; Pregnancy; Prenatal high-salt; progeny; Protein kinase C; Protein Kinase C - genetics; Protein Kinase C - metabolism; rats; Rats, Sprague-Dawley; risk; Signal Transduction; Sodium Chloride, Dietary - adverse effects; Up-Regulation; Vasoconstriction; Vasoconstriction - drug effects; young adults; Hypertension; Large-conductance Ca2+-activated K+ channels; Prenatal high-salt; Protein kinase C; Vasoconstriction
• ISSN: 1613-4125; 1613-4133
• DOI: 10.1002/mnfr.201400841

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 Ca²⁺, 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 Ca²⁺ 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.