ArticleAmerican journal of physiology. Lung cellular and molecular physiology2015
EET-dependent potentiation of pulmonary arterial pressure: sex-different regulation of soluble epoxide hydrolase.
Article in American journal of physiology. Lung cellular and molecular physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 18 citations in OpenAlex.
- Sex Difference of Alcoholic Hypertension: Mechanism and Targeted Therapy.Current hypertension reports · 2025Review
- Article
- Regulation of soluble epoxide hydrolase in renal-associated diseases: insights from potential mechanisms to clinical researches.Frontiers in endocrinology · 2024Review
- Roles of Genetic Predisposition in the Sex Bias of Pulmonary Pathophysiology, as a Function of Estrogens : Sex Matters in the Prevalence of Lung Diseases.Advances in experimental medicine and biology · 2021Article
- Estradiol Metabolism: Crossroads in Pulmonary Arterial Hypertension.International journal of molecular sciences · 2019Review
- Article
- Estrogen-dependent epigenetic regulation of soluble epoxide hydrolase via DNA methylation.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Sexually Dimorphic Regulation of EET Synthesis and Metabolism: Roles of Estrogen.Frontiers in pharmacology · 2018Article
- EETs promote hypoxic pulmonary vasoconstriction via constrictor prostanoids.American journal of physiology. Lung cellular and molecular physiology · 2017Article
- Sex-specific cardiopulmonary exercise testing indices related to hemodynamics in idiopathic pulmonary arterial hypertension.Therapeutic advances in respiratory disease · 2017Article
- Emerging concepts in smooth muscle contributions to airway structure and function: implications for health and disease.American journal of physiology. Lung cellular and molecular physiology · 2016Review
- Female-favorable attenuation of coronary myogenic constriction via reciprocal activations of epoxyeicosatrienoic acids and nitric oxide.American journal of physiology. Heart and circulatory physiology · 2016Article
- Sexually dimorphic adaptation of cardiac function: roles of epoxyeicosatrienoic acid and peroxisome proliferator-activated receptors.Physiological reports · 2016Article
- Reciprocal actions of constrictor prostanoids and superoxide in chronic hypoxia-induced pulmonary hypertension: roles of EETs.Pulmonary circulationArticle
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
We tested the hypothesis that suppression of epoxyeicosatrienoic acid (EET) metabolism via genetic knockout of the gene for soluble epoxide hydrolase (sEH-KO), or female-specific downregulation of sEH expression, plays a role in the potentiation of pulmonary hypertension. We used male (M) and female (F) wild-type (WT) and sEH-KO mice; the latter have high pulmonary EETs. Right ventricular systolic pressure (RVSP) and mean arterial blood pressure (MABP) in control and in response to in vivo administration of U46619 (thromboxane analog), 14,15-EET, and 14,15-EEZE [14,15-epoxyeicosa-5(z)-enoic acid; antagonist of EETs] were recorded. Basal RVSP was comparable among all groups of mice, whereas MABP was significantly lower in F-WT than M-WT mice and further reduced predominantly in F-KO compared with M-KO mice. U46619 dose dependently increased RVSP and MABP in all groups of mice. The increase in RVSP was significantly greater and coincided with smaller increases in MABP in M-KO and F-WT mice compared with M-WT mice. In F-KO mice, the elevation of RVSP by U46619 was even higher than in M-KO and F-WT mice, associated with the least increase in MABP. 14,15-EEZE prevented the augmentation of U46619-induced elevation of RVSP in sEH-KO mice, whereas 14,15-EET-induced pulmonary vasoconstriction was comparable in all groups of mice. sEH expression in the lungs was reduced, paralleled with higher levels of EETs in F-WT compared with M-WT mice. In summary, EETs initiate pulmonary vasoconstriction but act as vasodilators systemically. High pulmonary EETs, as a function of downregulation or deletion of sEH, potentiate U46619-induced increases in RVSP in a female-susceptible manner.
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