Evidence map›Paper›PMID 26277840›Full record

ArticleScientific reports2015

Chronic fetal exposure to caffeine altered resistance vessel functions via RyRs-BKCa down-regulation in rat offspring.

Na Li, Yongmei Li, Qinqin Gao, Dawei Li, Jiaqi Tang, Miao Sun, Pengjie Zhang, Bailin Liu, Caiping Mao, Zhice Xu

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

14 citing papers in PubMed, 26 citations in OpenAlex.

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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

10 authors at 3 institutions in 2 countries.

Na LiInstitute for Fetology, First Hospital of Soochow University, Suzhou, China.
Yongmei LiInstitute for Fetology, First Hospital of Soochow University, Suzhou, China.
Qinqin GaoInstitute for Fetology, First Hospital of Soochow University, Suzhou, China.
Dawei LiInstitute for Fetology, First Hospital of Soochow University, Suzhou, China.
Jiaqi TangInstitute for Fetology, First Hospital of Soochow University, Suzhou, China.
Miao SunInstitute for Fetology, First Hospital of Soochow University, Suzhou, China.
Pengjie ZhangInstitute for Fetology, First Hospital of Soochow University, Suzhou, China.
Bailin LiuInstitute for Fetology, First Hospital of Soochow University, Suzhou, China.
Caiping MaoInstitute for Fetology, First Hospital of Soochow University, Suzhou, China.
Zhice Xu1] Institute for Fetology, First Hospital of Soochow University, Suzhou, China [2] Center for Perinatal Biology, Loma Linda University, California, USA.
Soochow University · CNFirst Affiliated Hospital of Soochow University · CNLoma Linda University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Caffeine modifies vascular/cardiac contractility. Embryonic exposure to caffeine altered cardiac functions in offspring. This study determined chronic influence of prenatal caffeine on vessel functions in offspring. Pregnant Sprague-Dawley rats (5-month-old) were exposed to high dose of caffeine, their offspring (5-month-old) were tested for vascular functions in mesenteric arteries (MA) and ion channel activities in smooth muscle cells. Prenatal exposure to caffeine increased pressor responses and vasoconstrictions to phenylephrine, accompanied by enhanced membrane depolarization. Large conductance Ca2(+)-activated K(+) (BKCa) channels in buffering phenylephrine-induced vasoconstrictions was decreased, whole cell BKCa currents and spontaneous transient outward currents (STOCs) were decreased. Single channel recordings revealed reduced voltage/Ca(2+) sensitivity of BKCa channels. BKCa α-subunit expression was unchanged, BKCa β1-subunit and sensitivity of BKCa to tamoxifen were reduced in the caffeine offspring as altered biophysical properties of BKCa in the MA. Simultaneous [Ca(2+)]i fluorescence and vasoconstriction testing showed reduced Ca(2+), leading to diminished BKCa activation via ryanodine receptor Ca(2+) release channels (RyRs), causing enhanced vascular tone. Reduced RyR1 was greater than that of RyR3. The results suggest that the altered STOCs activity in the caffeine offspring could attribute to down-regulation of RyRs-BKCa, providing new information for further understanding increased risks of hypertension in developmental origins.

Indexed as

AnimalsBlood PressureBody WeightCaffeineCalciumCells, CulturedDown-RegulationFemaleLarge-Conductance Calcium-Activated Potassium ChannelsMaleMembrane PotentialsMesenteric ArteriesMyocytes, Smooth MusclePatch-Clamp TechniquesPeptidesPhenylephrineCaffeineCalciumiberiotoxinLarge-Conductance Calcium-Activated Potassium ChannelsPeptidesPhenylephrineRyanodine Receptor Calcium Release ChannelTamoxifen

Identifiers

PMID26277840
PMCPMC4642531
OpenAlexW2402493872

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Registered trials

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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.