ArticleEarly human development2011
Fetal programming of adult hypertension in female rat offspring exposed to androgens in utero.
Article in Early human development, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 59 citations in OpenAlex.
- Impaired glucose tolerance and insulin resistance in a prenatally-androgenized rat model of polycystic ovary syndrome in later life.Experimental physiology · 2025Article
- Maternal androgen excess increases the risk of metabolic syndrome in female offspring in their later life: A long-term population-based follow-up study.Archives of gynecology and obstetrics · 2023Article
- Developmental programming: adverse sexually dimorphic transcriptional programming of gestational testosterone excess in cardiac left ventricle of fetal sheep.Scientific reports · 2023Article
- Elevated Maternal Testosterone Levels Alter PFOA Elimination and Tissue Distribution in Pregnant Rats.Journal of environmental science and public health · 2023Article
- Cardiovascular Dysfunction in Intrauterine Growth Restriction.Current hypertension reports · 2022Review
- Cardiovascular disease risk in offspring of polycystic ovary syndrome.Frontiers in endocrinology · 2022Review
- MEHP induces alteration of mitochondrial function and inhibition of steroid biosynthesis in MA-10 mouse tumor Leydig cells.Toxicology · 2021Article
- Preeclampsia and Cardiovascular Risk for Offspring.Journal of clinical medicine · 2021Review
- Activation of angiotensin type 2 receptor attenuates testosterone-induced hypertension and uterine vascular resistance in pregnant rats†.Biology of reproduction · 2021Article
- Current Updates on Pre-eclampsia: Maternal and Foetal Cardiovascular Diseases Predilection, Science or Myth? : Future cardiovascular disease risks in mother and child following pre-eclampsia.Current hypertension reports · 2021Review
- Article
- Animal Models to Understand the Etiology and Pathophysiology of Polycystic Ovary Syndrome.Endocrine reviews · 2020Review
- Vascular Pathways of Testosterone: Clinical Implications.Journal of cardiovascular translational research · 2020Review
- Lasting Effects of Intrauterine Exposure to Preeclampsia on Offspring and the Underlying Mechanism.AJP reports · 2019Review
- Redox regulation of hormone sensitive lipase: Potential role in the mechanism of MEHP-induced stimulation of basal steroid synthesis in MA-10 Leydig cells.Reproductive toxicology (Elmsford, N.Y.) · 2019Article
- Sex Differences in the Prenatal Programming of Adult Metabolic Syndrome by Maternal Androgens.The Journal of clinical endocrinology and metabolism · 2018Article
- Androgens in maternal vascular and placental function: implications for preeclampsia pathogenesisReproduction (Cambridge, England) · 2018Review
- Elevated androgen levels induce hyperinsulinemia through increase in Ins1 transcription in pancreatic beta cells in female rats.Biology of reproduction · 2018Article
- Hyperandrogenemia reduces endothelium-derived hyperpolarizing factor-mediated relaxation in mesenteric artery of female rats.Biology of reproduction · 2017Article
- Prenatal Testosterone Exposure Decreases Aldosterone Production but Maintains Normal Plasma Volume and Increases Blood Pressure in Adult Female Rats.Biology of reproduction · 2016Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
aimsThe influence of prenatal factors on the development of arterial hypertension has gained considerable interest in recent years. We examined the effects of prenatal testosterone treatment on blood pressure in adult female rats. Further, to define the mechanisms whereby blood pressure may be raised, we examined vascular endothelial function and nitric oxide synthesis. METHODS AND
resultsTestosterone propionate (0.5 mg/kg/day; SC) or vehicle was administered to pregnant Sprague-Dawley rats from gestational day 15-19. Maternal feed intake and plasma levels of steroid hormones were measured in the dams. In the female offspring, birth weight, growth rate, blood pressure, vascular reactivity, eNOS expression, and nitric oxide production were examined. In the pregnant rats, testosterone-treatment increased plasma testosterone levels by 2-fold without any significant changes in 17β-estradiol, progesterone and corticosterone levels. Testosterone-treatment did not affect maternal feed intake. The pups born to testosterone mothers were smaller in size but exhibited catch-up growth. The blood pressure in the testosterone offspring at 6 months of age was significantly higher compared to controls. Endothelium-intact mesenteric arteries from testosterone group exhibited increased contractile responses to phenylephrine, decreased vasodilation to acetylcholine and unaltered responses to sodium nitroprusside in comparison to control rats. Testosterone rats demonstrated decreased expression for eNOS, and reduced nitric oxide production.
conclusionsOur data show that elevated plasma maternal testosterone levels: (1) causes low birth weight followed by catch-up growth and hypertension in female offspring and (2) alters endothelium-dependent vascular responses. The endothelial dysfunction is associated with decreased activity/expression of eNOS.
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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.