ArticleAmerican journal of physiology. Endocrinology and metabolism2015
Functional changes in the uterine artery precede the hypertensive phenotype in a transgenic model of hypertensive pregnancy.
Article in American journal of physiology. Endocrinology and metabolism, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.
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Who cites it
8 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.
- Guidelines for assessing maternal cardiovascular physiology during pregnancy and postpartum.American journal of physiology. Heart and circulatory physiology · 2024Guideline
- Sex differences in middle cerebral artery reactivity and hemodynamics independent from changes in systemic arterial stiffness in Sprague-Dawley rats.Physiological reports · 2025Article
- Vascular changes in the cycling and early pregnant uterus.JCI insight · 2023Review
- Maternal PUFAs, Placental Epigenetics, and Their Relevance to Fetal Growth and Brain Development.Reproductive sciences (Thousand Oaks, Calif.) · 2023Review
- Evidence of Nitric Oxide Impairment During Hypertensive Pregnancies.Advances in experimental medicine and biology · 2023Review
- Bisphenol a Interferes with Uterine Artery Features and Impairs Rat Feto-Placental Growth.International journal of molecular sciences · 2021Article
- Sex differences in vascular reactivity in mesenteric arteries from a mouse model of acute intermittent porphyria.Molecular genetics and metabolism · 2019Article
- Intermittent hypoxia impairs uterine artery function in pregnant mice.The Journal of physiology · 2019Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 3 countries.
Funding
Abstract
The pregnant female human angiotensinogen (hAGN) transgenic rat mated with the male human renin (hREN) transgenic rat is a model of preeclampsia (TgA) with increased blood pressure, proteinuria, and placenta alterations of edema and necrosis at late gestation. We studied vascular responses and the role of COX-derived prostanoids in the uterine artery (UA) at early gestation in this model. TgA UA showed lower stretch response, similar smooth muscle α-actin content, and lower collagen content compared with Sprague-Dawley (SD) UA. Vasodilation to acetylcholine was similar in SD and TgA UA (64 ± 8 vs. 75 ± 6% of relaxation, P > 0.05), with an acetylcholine-induced contraction in TgA UA that was abolished by preincubation with indomethacin (78 ± 6 vs. 83 ± 11%, P > 0.05). No differences in the contraction to phenylephrine were observed (159 ± 11 vs. 134 ± 12 %KMAX, P > 0.05), although in TgA UA this response was greatly affected by preincubation with indomethacin (179 ± 16 vs. 134 ± 9 %KMAX, P < 0.05, pD2 5.92 ± 0.08 vs. 5.85 ± 0.03, P < 0.05). Endothelium-independent vasodilation was lower in TgA UA (92 ± 2 vs. 74 ± 5% preconstricted tone, P < 0.05), and preincubation with indomethacin restored the response to normal values (90 ± 3 vs. 84 ± 3%). Immunostaining showed similar signals for α-actin, COX-2, and eNOS between groups (P > 0.05). Plasma thromboxane levels were similar between groups. In summary, TgA UA displays functional alterations at early gestation before the preeclamptic phenotype is established. Inhibition of COX enzymes normalizes some of the functional defects in the TgA UA. An increased role for COX-derived prostanoids in this model of preeclampsia may contribute to the development of a hypertensive pregnancy.
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Registered trials
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