ArticleAmerican journal of physiology. Regulatory, integrative and comparative physiology2008
Selective estrogen receptor-alpha and estrogen receptor-beta agonists rapidly decrease pulmonary artery vasoconstriction by a nitric oxide-dependent mechanism.
Article in American journal of physiology. Regulatory, integrative and comparative physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 73 citations in OpenAlex.
- Aging is associated with altered estrogen receptor expression and alters redox protein balance in human female skeletal muscle.GeroScience · 2026Article
- Sex-specific insights in atherosclerosis and pulmonary arterial hypertension: an overlooked comorbidity.Frontiers in cardiovascular medicine · 2026Review
- Sex differences in pulmonary (arterial) hypertension: does it matter?Current opinion in pulmonary medicine · 2025Review
- Hydroxy-Safflower Yellow A Mitigates Vascular Remodeling in Rat Pulmonary Arterial Hypertension.Drug design, development and therapy · 2024Article
- Role of estrogen receptors in health and disease.Frontiers in endocrinology · 2022Review
- Sex and gender in pulmonary arterial hypertension.European respiratory review : an official journal of the European Respiratory Society · 2021Review
- Estrogens and the regulation of glucose metabolism.World journal of diabetes · 2021Review
- Pulmonary Hypertension in Pregnancy: A Review.Medicina (Kaunas, Lithuania) · 2021Review
- Sex Differences in Pulmonary Hypertension.Frontiers in aging · 2021Review
- Sex Differences, Estrogen Metabolism and Signaling in the Development of Pulmonary Arterial Hypertension.Frontiers in cardiovascular medicine · 2021Review
- 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
- The Role of Estrogen Receptors in Cardiovascular Disease.International journal of molecular sciences · 2020Review
- Sex, Gender, and Sex Hormones in Pulmonary Hypertension and Right Ventricular Failure.Comprehensive Physiology · 2019Review
- Hypoxia Upregulates Estrogen Receptor β in Pulmonary Artery Endothelial Cells in a HIF-1α-Dependent Manner.American journal of respiratory cell and molecular biology · 2018Article
- miRNA as a New Regulatory Mechanism of Estrogen Vascular Action.International journal of molecular sciences · 2018Review
- Role of miRNA in the Regulatory Mechanisms of Estrogens in Cardiovascular Ageing.Oxidative medicine and cellular longevity · 2018Review
- Estrogen receptor-dependent attenuation of hypoxia-induced changes in the lung genome of pulmonary hypertension rats.Pulmonary circulation · 2017Article
- 17β-Estradiol mediates superior adaptation of right ventricular function to acute strenuous exercise in female rats with severe pulmonary hypertension.American journal of physiology. Lung cellular and molecular physiology · 2016Article
- Identification of Differential ER-Alpha Versus ER-Beta Mediated Activation of eNOS in Ovine Uterine Artery Endothelial Cells.Biology of reproduction · 2016Article
- EET-dependent potentiation of pulmonary arterial pressure: sex-different regulation of soluble epoxide hydrolase.American journal of physiology. Lung cellular and molecular physiology · 2015Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Both endogenous and exogenous estrogen decrease pulmonary artery (PA) vasoconstriction. Whether these effects are mediated via estrogen receptor (ER)-alpha or ER-beta, and whether the contribution of ERs is stimulus-dependent, remains unknown. We hypothesized that administration of the selective ER-alpha agonist propylpyrazole triol (PPT) and/or the selective ER-beta agonist diarylpropiolnitrile (DPN) rapidly decreases PA vasoconstriction induced by pharmacologic and hypoxic stimuli via a nitric oxide (NO)-dependent mechanism. PA rings (n = 3-10/group) from adult male Sprague-Dawley rats were suspended in physiologic organ baths. Force displacement was measured. Vasoconstrictor responses to phenylephrine (10(-8)M - 10(-5)M) and hypoxia (Po(2) 35-45 mmHg) were determined. Endothelium-dependent and -independent vasorelaxation were measured by generating dose-response curves to acetylcholine (10(-8)M - 10(-4)M) and sodium nitroprusside (10(-9)M - 10(-5)M). PPT or DPN (10(-9)M - 5 x 10(-5)M) were added to the organ bath in the presence and absence of the NO-synthase inhibitor N(omega)-nitro-l-arginine methyl ester (l-NAME) (10(-4)M). Selective ER-alpha activation (PPT, 5 x 10(-5)M) rapidly (<20 min) decreased phenylephrine-induced vasoconstriction. This effect, as well as PPT's effects on endothelium-dependent vasorelaxation, were neutralized by l-NAME. In contrast, selective ER-beta activation (DPN, 5 x 10(-5)M) rapidly decreased phase II of hypoxic pulmonary vasoconstriction (HPV). l-NAME eliminated this phenomenon. Lower PPT or DPN concentrations were less effective. We conclude that both ER-alpha and ER-beta decrease PA vasoconstriction. The immediate onset of effect suggests a nongenomic mechanism. The contribution of specific ERs appears to be stimulus specific, with ER-alpha primarily modulating phenylephrine-induced vasoconstriction, and ER-beta inhibiting HPV. NO inhibition eliminates these effects, suggesting a central role for NO in mediating the pulmonary vascular effects of both ER-alpha and ER-beta.
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Registered trials
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