Why the study?
Does prenatal exposure to maternal high-salt diets alter pressor responses and microvessel functions in adult rat offspring?
Does prenatal exposure to maternal high-salt diets alter pressor responses and microvessel functions in adult rat offspring?
Prenatal exposure to high-salt diets alters microvascular activity in adult rat offspring via PKC/BK signaling pathways, potentially increasing hypertension risk.
Answers are grounded in this paper and cite their sources.
Alerts to possible intergenerational hypertension risk from maternal diet; extends developmental origins research but remains hypothesis-generating pending human data.
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.
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Bo et al. (2015) studied this question.
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