Evidence map›Paper›PMID 30102356›Full record

ArticleBiology of reproduction2019

Testosterone plays a permissive role in angiotensin II-induced hypertension and cardiac hypertrophy in male rats.

Jay S Mishra, Amar S More, Kathirvel Gopalakrishnan, Sathish Kumar

Abstract read
In one paragraph

Article in Biology of reproduction, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

38 citing papers in PubMed, 66 citations in OpenAlex.

  1. Trial
  2. Trial
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  7. Observational
  8. Article
  9. Article
  10. Article
  11. Effect of Pituitary-Target Gland Axis on RAAS in the Context of COVID-19.International journal of medical sciences · 2025
    Review
  12. Article
  13. Article
  14. Revisiting sex as a biological variable in hypertension research.The Journal of clinical investigation · 2024
    Review
  15. Chronic intermittent hypoxia-induced hypertension: the impact of sex hormones.American journal of physiology. Regulatory, integrative and comparative physiology · 2024
    Review
  16. Article
  17. Characterization of a robust mouse model of heart failure with preserved ejection fraction.American journal of physiology. Heart and circulatory physiology · 2023
    Article
  18. Review
  19. Article
  20. Article
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

4 authors at 2 institutions in 1 country.

Jay S MishraDepartment of Comparative Biosciences, University of Wisconsin-Madison, Madison, Wisconsin, USA.
Amar S MoreDepartment of Obstetrics and Gynecology, University of Texas Medical Branch, Galveston, Texas, USA.
Kathirvel GopalakrishnanDepartment of Comparative Biosciences, University of Wisconsin-Madison, Madison, Wisconsin, USA.
Sathish KumarDepartment of Comparative Biosciences, University of Wisconsin-Madison, Madison, Wisconsin, USA.
University of Wisconsin–Madison · USThe University of Texas Medical Branch at Galveston · US

Funding

Sex-specific fetal programming of adult vascular dysfunction and hypertensionR01HL119869 · NHLBI · UNIVERSITY OF WISCONSIN-MADISON · PI KUMAR, SATHISH · 2013 to 2017
$1.9M
Vascular AT2R expression and function during pregnancyR01HL134779 · NHLBI · UNIVERSITY OF WISCONSIN-MADISON · PI KUMAR, SATHISH · 2017 to 2020
$1.5M
NHLBI NIH HHS R01 HL119869NHLBI NIH HHS R01 HL134779
6 · The paper itself

Abstract

Sex hormones contribute to sex differences in blood pressure. Inappropriate activation of the renin-angiotensin system is involved in vascular dysfunction and hypertension. This study evaluated the role of androgens (testosterone) in angiotensin II (Ang II)-induced increase in blood pressure, vascular reactivity, and cardiac hypertrophy. Eight-week-old male Wistar rats underwent sham operation, castration, or castration with testosterone replacement. After 12 weeks of chronic changes in androgen status, Ang II (120 ng/kg per minute) or saline was infused for 28 days via subcutaneous miniosmotic pump, and changes in blood pressure was measured. Vascular reactivity and Ang II receptor levels were examined in mesenteric arteries. Heart weight, cardiac ANP mRNA levels, and fibrosis were also assessed. Ang II infusion increased arterial pressure in intact males. The Ang II-induced increase in hypertensive response was prevented in castrated males. Testosterone replacement in castrated males restored Ang II-induced hypertensive responses. Castration reduced vascular AT1R/AT2R ratio, an effect that was reversed by testosterone replacement. Ang II-induced hypertension was associated with increased contractile response of mesenteric arteries to Ang II and phenylephrine in intact and testosterone-replaced castrated males; these increases were prevented in castrated males. Ang II infusion induced increased left ventricle-to-body weight ratio and ANP mRNA expression, indicators of left ventricular hypertrophy, and fibrosis in intact and testosterone-replaced castrated males, and castration prevented the increase in these parameters caused by Ang II. This study demonstrates that testosterone plays a permissive role in development and maintenance of Ang II-induced vascular dysfunction, hypertension, and cardiac hypertrophy.

Indexed as

Angiotensin IIAnimalsAtrial Natriuretic FactorCardiomegalyHypertensionMaleMesenteric ArteriesOrchiectomyRatsRats, WistarReceptors, AndrogenReceptors, AngiotensinRenin-Angiotensin SystemTestosteroneAngiotensin IIAtrial Natriuretic FactorReceptors, AndrogenReceptors, AngiotensinTestosterone

Identifiers

PMID30102356
PMCPMC6335213
OpenAlexW2887512841

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.