Evidence map›Paper›PMID 26224008›Full record

ArticleBiology of reproduction2015

Antenatal Antioxidant Prevents Nicotine-Mediated Hypertensive Response in Rat Adult Offspring.

DaLiao Xiao, Xiaohui Huang, Yong Li, Chiranjib Dasgupta, Lei Wang, Lubo Zhang

Open access · bronzeAbstract read
In one paragraph

Article in Biology of reproduction, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
5.7field-weighted citation impact, top 5% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

35 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.

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  19. Early-Life Origins of Metabolic Syndrome: Mechanisms and Preventive Aspects.International journal of molecular sciences · 2021
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

DaLiao XiaoCenter for Perinatal Biology, Department of Basic Sciences, Loma Linda University School of Medicine, Loma Linda, California Dxiao@llu.edu.
Xiaohui HuangCenter for Perinatal Biology, Department of Basic Sciences, Loma Linda University School of Medicine, Loma Linda, California.
Yong LiCenter for Perinatal Biology, Department of Basic Sciences, Loma Linda University School of Medicine, Loma Linda, California.
Chiranjib DasguptaCenter for Perinatal Biology, Department of Basic Sciences, Loma Linda University School of Medicine, Loma Linda, California.
Lei WangCenter for Perinatal Biology, Department of Basic Sciences, Loma Linda University School of Medicine, Loma Linda, California.
Lubo ZhangCenter for Perinatal Biology, Department of Basic Sciences, Loma Linda University School of Medicine, Loma Linda, California.
Loma Linda University · US

Funding

Hypoxia and Aberrant Uterine Vascular Adaptation in PregnancyR01HL110125 · NHLBI · LOMA LINDA UNIVERSITY · PI ZHANG, LUBO · 2011 to 2015
$1.8M
Developmental Programming of Ischemic-Sensitive Phenotype in the HeartR01HL118861 · NHLBI · LOMA LINDA UNIVERSITY · PI ZHANG, LUBO · 2014 to 2017
$1.8M
Fetal Programming of Vascular Dysfunction by Nicotine ExposureR03DA032510 · NIDA · LOMA LINDA UNIVERSITY · PI XIAO, DALIAO · 2011 to 2012
$74k
NHLBI NIH HHS HL118861NHLBI NIH HHS R01 HL110125NHLBI NIH HHS R01 HL118861NIDA NIH HHS DA032510NIDA NIH HHS R03 DA032510
6 · The paper itself

Abstract

Previous studies have demonstrated that perinatal nicotine exposure increased blood pressure (BP) in adult offspring. However, the underlying mechanisms were unclear. The present study tested the hypothesis that perinatal nicotine-induced programming of hypertensive response is mediated by enhanced reactive oxygen species (ROS) in the vasculature. Nicotine was administered to pregnant rats via subcutaneous osmotic mini-pumps from Day 4 of gestation to Day 10 after birth, in the absence or presence of the ROS inhibitor N-acetyl-cysteine (NAC) in the drinking water. Experiments were conducted in 8-mo-old male offspring. Perinatal nicotine treatment resulted in a significant increase in arterial ROS production in offspring, which was abrogated by NAC. Angiotensin II (Ang II)-induced BP responses were significantly higher in nicotine-treated group than in saline-treated control group, and NAC treatment blocked the nicotine-induced increase in BP response. Consistent with that, the nicotine treatment significantly increased both Ang II-induced and phorbol [12, 13]-dibutyrate (PDBu, a Prkc activator)-induced arterial contractions in adult offspring, which were blocked by NAC treatment. In addition, perinatal nicotine treatment significantly attenuated acetylcholine-induced arterial relaxation in offspring, which was also inhibited by NAC treatment. Results demonstrate that inhibition of ROS blocks the nicotine-induced increase in arterial reactivity and BP response to vasoconstrictors in adult offspring, suggesting a key role for increased oxidative stress in nicotine-induced developmental programming of hypertensive phenotype in male offspring.

Indexed as

AcetylcysteineAngiotensin IIAnimalsAntioxidantsBody WeightEnzyme ActivationFemaleHumansHypertensionMuscle RelaxationMuscle, Smooth, VascularNicotineNicotinic AgonistsPhorbol 12,13-DibutyratePregnancyPrenatal Exposure Delayed EffectsAcetylcysteineAngiotensin IIAntioxidantsNicotineNicotinic AgonistsPhorbol 12,13-DibutyrateProtein Kinase CReactive Oxygen Speciesantioxidantblood pressureperinatal nicotineprogrammingvascular dysfunction

Identifiers

PMID26224008
PMCPMC4710188
OpenAlexW1821454695

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.