Evidence map›Paper›PMID 24842922›Full record

ArticleHypertension (Dallas, Tex. : 1979)2014

Elevated testosterone levels during rat pregnancy cause hypersensitivity to angiotensin II and attenuation of endothelium-dependent vasodilation in uterine arteries.

Vijayakumar Chinnathambi, Chellakkan S Blesson, Kathleen L Vincent, George R Saade, Gary D Hankins, Chandra Yallampalli, Kunju Sathishkumar

Abstract read
In one paragraph

Article in Hypertension (Dallas, Tex. : 1979), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
–field-weighted citation impact
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

44 citing papers in PubMed.

  1. Article
  2. Article
  3. Reduced ATHypertension (Dallas, Tex. : 1979) · 2025
    Article
  4. Review
  5. Article
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  16. Article
  17. CaInternational journal of molecular sciences · 2023
    Review
  18. Article
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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

7 authors.

Vijayakumar ChinnathambiFrom the Division of Reproductive Endocrinology, Department of Obstetrics and Gynecology, University of Texas Medical Branch, Galveston (V.C., K.L.V., G.R.S., G.D.H., K.S.); and Department of Obstetrics and Gynecology, Baylor College of Medicine, Houston, TX (C.S.B., C.Y.).
Chellakkan S BlessonFrom the Division of Reproductive Endocrinology, Department of Obstetrics and Gynecology, University of Texas Medical Branch, Galveston (V.C., K.L.V., G.R.S., G.D.H., K.S.); and Department of Obstetrics and Gynecology, Baylor College of Medicine, Houston, TX (C.S.B., C.Y.).
Kathleen L VincentFrom the Division of Reproductive Endocrinology, Department of Obstetrics and Gynecology, University of Texas Medical Branch, Galveston (V.C., K.L.V., G.R.S., G.D.H., K.S.); and Department of Obstetrics and Gynecology, Baylor College of Medicine, Houston, TX (C.S.B., C.Y.).
George R SaadeFrom the Division of Reproductive Endocrinology, Department of Obstetrics and Gynecology, University of Texas Medical Branch, Galveston (V.C., K.L.V., G.R.S., G.D.H., K.S.); and Department of Obstetrics and Gynecology, Baylor College of Medicine, Houston, TX (C.S.B., C.Y.).
Gary D HankinsFrom the Division of Reproductive Endocrinology, Department of Obstetrics and Gynecology, University of Texas Medical Branch, Galveston (V.C., K.L.V., G.R.S., G.D.H., K.S.); and Department of Obstetrics and Gynecology, Baylor College of Medicine, Houston, TX (C.S.B., C.Y.).
Chandra YallampalliFrom the Division of Reproductive Endocrinology, Department of Obstetrics and Gynecology, University of Texas Medical Branch, Galveston (V.C., K.L.V., G.R.S., G.D.H., K.S.); and Department of Obstetrics and Gynecology, Baylor College of Medicine, Houston, TX (C.S.B., C.Y.).
Kunju SathishkumarFrom the Division of Reproductive Endocrinology, Department of Obstetrics and Gynecology, University of Texas Medical Branch, Galveston (V.C., K.L.V., G.R.S., G.D.H., K.S.); and Department of Obstetrics and Gynecology, Baylor College of Medicine, Houston, TX (C.S.B., C.Y.). kusathis@utmb.edu.

Funding

SEX STEROID HORMONES AND CALCITONIN GENE RELATED PEPTIDER01HL058144 · NHLBI · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI CHAUHAN, MADHU LATA S., YALLAMPALLI, CHANDRASEKHAR · 1998 to 2022
$6.9M
Sex-specific fetal programming of adult vascular dysfunction and hypertensionR01HL119869 · NHLBI · UNIVERSITY OF WISCONSIN-MADISON · PI KUMAR, SATHISH · 2013 to 2017
$1.9M
Developmental programming: influence of sex steroids and mechanismsR01HL102866 · NHLBI · UNIVERSITY OF TEXAS MED BR GALVESTON · PI YALLAMPALLI, CHANDRASEKHAR · 2011 to 2014
$1.5M
Maternal Androgen Excess: Vascular and Placental Function and Fetal ConsequencesR03HD069750 · NICHD · UNIVERSITY OF TEXAS MED BR GALVESTON · PI KUMAR, SATHISH · 2011 to 2012
$153k
NHLBI NIH HHS HL102866NHLBI NIH HHS HL119869NHLBI NIH HHS HL 58144NHLBI NIH HHS R01 HL058144NHLBI NIH HHS R01 HL102866NHLBI NIH HHS R01 HL119869NICHD NIH HHS HD069750NICHD NIH HHS R03 HD069750
6 · The paper itself

Abstract

Elevated testosterone levels increase maternal blood pressure and decrease uterine blood flow in pregnancy, resulting in abnormal perinatal outcomes. We tested whether elevated testosterone alters uterine artery adaptations during pregnancy, and whether these alterations depend on endothelium-derived factors such as nitric oxide, endothelium-derived hyperpolarizing factor, and prostacyclin, or endothelium-independent mechanisms such as angiotensin II (Ang-II). Pregnant Sprague-Dawley rats were injected with vehicle (n=20) or testosterone propionate (0.5 mg/kg per day from gestation day 15 to 19; n=20). Plasma testosterone levels increased 2-fold in testosterone-injected rats compared with controls. Elevated testosterone significantly decreased placental and pup weights compared with controls. In endothelium-intact uterine arteries, contractile responses to thromboxane, phenylephrine, and Ang-II were greater in testosterone-treated rats compared with controls. In endothelium-denuded arteries, contractile responses to Ang-II (pD2=9.1±0.04 versus 8.7±0.04 in controls; P<0.05), but not thromboxane and phenylephrine, were greater in testosterone-treated rats. Ang-II type 1b receptor expression was increased, whereas Ang-II type 2 receptor was decreased in testosterone-exposed arteries. In endothelium-denuded arteries, relaxations to sodium nitroprusside were unaffected. Endothelium-dependent relaxation to acetylcholine was significantly lower in arteries from testosterone-treated dams (Emax=51.80±6.9% versus 91.98±1.4% in controls; P<0.05). The assessment of endothelial factors showed that nitric oxide-, endothelium-derived hyperpolarizing factor-, and prostacyclin-mediated relaxations were blunted in testosterone-treated dams. Endothelial nitric oxide synthase, small conductance calcium-activated potassium channel-3, and prostacyclin receptor expressions were significantly decreased in arteries from testosterone-treated dams. Hypoxia-inducible factor-1α, Ankrd37, and Egln were significantly increased in testosterone-exposed placentas. These results suggest that elevated maternal testosterone impairs uterine vascular function, which may lead to an increased vascular resistance and a decrease in uterine blood flow.

Indexed as

AcetylcholineAngiotensin IIAnimalsBlood PressureEndothelium, VascularFemaleNitroprussidePregnancyRatsRats, Sprague-DawleyTestosteroneUterine ArteryVasodilationAcetylcholineAngiotensin IINitroprussideTestosteroneendothelium-dependent hyperpolarization factorfetal developmentnitric oxideprostacyclinuterine arteryvasoconstrictionvasodilation

Identifiers

PMID24842922
PMCPMC4096063

What OpenQuestion holds

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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.