ArticleClinical science (London, England : 1979)2019
Prenatal cold exposure causes hypertension in offspring by hyperactivity of the sympathetic nervous system.
Article in Clinical science (London, England : 1979), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed, 19 citations in OpenAlex.
- Advancing entropy analysis for heart rate variability: clinical insights for aging and diabetes.Frontiers in physiology · 2026Review
- Cold exposure and the cardiovascular system: from physiological adaptation to pathological risk.Frontiers in physiology · 2025Review
- GR/Ahi1 regulates WDR68-DYRK1A binding and mediates cognitive impairment in prenatally stressed offspring.Cellular and molecular life sciences : CMLS · 2024Article
- Synergistic Effect of Uroguanylin and DJournal of the American Heart Association · 2022Article
- Paternal long-term PM2.5 exposure causes hypertension via increased renal AT1R expression and function in male offspring.Clinical science (London, England : 1979) · 2021Article
- Characterization of Gut Microbiota in Prenatal Cold Stress Offspring Rats by 16S rRNA Sequencing.Animals : an open access journal from MDPI · 2020Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Environmental temperature plays a role in the variation of blood pressure. Maternal cold stress could affect the physiological phenotype of the offspring, including blood pressure elevation. In the present study, we found that adult offspring of dams exposed to cold have increased systolic and diastolic blood pressure, and decreased urine volume and sodium excretion, accompanied by increased heart rate and heart rate variability, secondary to increased activity of the sympathetic nervous system. Renal denervation or adrenergic receptor blockade decreased blood pressure and increased sodium excretion. The increase in peripheral sympathetic nerve activity can be ascribed to the central nervous system because administration of clonidine, a centrally acting α
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