ArticleBiology of reproduction2013
Prenatal testosterone induces sex-specific dysfunction in endothelium-dependent relaxation pathways in adult male and female rats.
Article in Biology of reproduction, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.
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Who cites it
22 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.
- The role of fetal heart rate in first trimester sonograms in prediction of fetal sex: a systematic review and meta-analysis.BMC pregnancy and childbirth · 2023Pooled it
- Elevated maternal testosterone induces sex-specific neurodevelopmental changes and ASD-related behavioral phenotypes in rat offspring.Pediatric research · 2026Article
- Sex differences in the sensitization of prenatally programmed hypertension.Frontiers in physiology · 2025Review
- Associations of central precocious puberty with blood pressure trajectories: prospective cohort study.Pediatric research · 2024Article
- Cardiovascular disease risk in offspring of polycystic ovary syndrome.Frontiers in endocrinology · 2022Review
- The potential role of testosterone in hypertension and target organ damage in hypertensive postmenopausal women.Clinical interventions in aging · 2019Article
- 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
- Endothelium-Dependent Hyperpolarization (EDH) in Hypertension: The Role of Endothelial Ion Channels.International journal of molecular sciences · 2018Review
- Hyperandrogenemia reduces endothelium-derived hyperpolarizing factor-mediated relaxation in mesenteric artery of female rats.Biology of reproduction · 2017Article
- Postnatal Cardiovascular Consequences in the Offspring of Pregnant Rats Exposed to Smoking and Smoking Cessation Pharmacotherapies.Reproductive sciences (Thousand Oaks, Calif.) · 2017Article
- Patient-Specific iPSC-Derived Endothelial Cells Uncover Pathways that Protect against Pulmonary Hypertension in BMPR2 Mutation Carriers.Cell stem cell · 2017Article
- Prenatal Testosterone Exposure Decreases Aldosterone Production but Maintains Normal Plasma Volume and Increases Blood Pressure in Adult Female Rats.Biology of reproduction · 2016Article
- Elevated Testosterone Reduces Uterine Blood Flow, Spiral Artery Elongation, and Placental Oxygenation in Pregnant Rats.Hypertension (Dallas, Tex. : 1979) · 2016Article
- Reactive oxygen species: players in the cardiovascular effects of testosterone.American journal of physiology. Regulatory, integrative and comparative physiology · 2016Review
- Prenatal Testosterone Exposure Leads to Gonadal Hormone-Dependent Hyperinsulinemia and Gonadal Hormone-Independent Glucose Intolerance in Adult Male Rat Offspring.Biology of reproduction · 2016Article
- Long Lasting Microvascular Tone Alteration in Rat Offspring Exposed In Utero to Maternal Hyperglycaemia.PloS one · 2016Article
- In utero origin of sex-related differences in future cardiovascular disease.Biology of sex differences · 2016Article
- Enalapril Normalizes Endothelium-Derived Hyperpolarizing Factor-Mediated Relaxation in Mesenteric Artery of Adult Hypertensive Rats Prenatally Exposed to Testosterone.Biology of reproduction · 2015Article
- Prenatal testosterone exposure induces hypertension in adult females via androgen receptor-dependent protein kinase Cδ-mediated mechanism.Hypertension (Dallas, Tex. : 1979) · 2015Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Prenatal testosterone (T) exposure impacts postnatal cardiovascular function, leading to increases in blood pressure with associated decreased endothelium-dependent vascular relaxation in adult females. Endothelial function in males is not known. Furthermore, which of the endothelial pathways contributes to endothelial dysfunction and if there exists sex differences are not known. The objective of this study was to characterize the relative contribution of nitric oxide (NO) and endothelium-derived hyperpolarizing factor (EDHF) to the impaired endothelium-dependent vasodilation in prenatal T-exposed adult males and females. Offspring of pregnant rats treated with T propionate or its vehicle were examined. Telemetric blood pressure levels and endothelium-dependent vascular reactivity were assessed with wire myography. Levels of nitric oxide synthase (NOS3) and Kcnn3 and Kcnn4 channel expression were examined in mesenteric arteries. Mean arterial pressure was significantly higher in T males and females than in controls. Endothelium-dependent acetylcholine relaxation was significantly lower in both T males and females. EDHF-mediated relaxation was specifically blunted in T males (Emax = 48.64% ± 3.73%) compared to that in control males (Emax = 81.71% ± 3.18%); however, NO-mediated relaxation was specifically impaired in T females (Emax = 36.01% ± 4.29%) compared with that in control females (Emax = 54.56% ± 6.37%). Relaxation to sodium nitroprusside and levcromakalim were unaffected with T-treatment. NOS3 protein was decreased in T females but not in T males. Kcnn3 expression was decreased in both T males and females compared to controls. These findings suggest that prenatal T leads to an increase in blood pressure in the adult offspring, associated with blunting of endothelial cell-associated relaxation and that the effects are sex-specific: EDHF-related in males and NO-related in females.
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Registered trials
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