ArticleSteroids2014
Vasodilation by GPER in mesenteric arteries involves both endothelial nitric oxide and smooth muscle cAMP signaling.
Article in Steroids, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
63 citing papers in PubMed, 109 citations in OpenAlex.
- Ovarian hormones moderate systolic hypertension in femaleAmerican journal of physiology. Renal physiology · 2026Article
- Ovarian Hormones Moderate Systolic Hypertension in FemalebioRxiv : the preprint server for biology · 2025Article
- The machinery of healthy vasoconstriction: an overview.Pflugers Archiv : European journal of physiology · 2025Review
- Sex-specific effects of exogenous asparagine on colorectal tumor growth, 17β-estradiol levels, and aromatase.Pharmacological research · 2025Article
- LNS8801: An Enantiomerically Pure Agonist of the G Protein-Coupled Estrogen Receptor Suitable for Clinical Development.Cancer research communications · 2025Article
- GPER expression prevents estrogen-induced urinary retention in obese mice.The Journal of steroid biochemistry and molecular biology · 2024Article
- Activation of G Protein-Coupled Estrogen Receptor (GPER) Negatively Modulates Cardiac Excitation-Contraction Coupling (ECC) through the PI3K/NOS/NO Pathway.International journal of molecular sciences · 2024Article
- Ovariectomy-Induced Arterial Stiffening Differs From Vascular Aging and Is Reversed by GPER Activation.Hypertension (Dallas, Tex. : 1979) · 2024Article
- The Role of G Protein-Coupled Estrogen Receptor (GPER) in Vascular Pathology and Physiology.Biomolecules · 2023Review
- LNS8801 inhibits Acute Myeloid Leukemia by Inducing the Production of Reactive Oxygen Species and Activating the Endoplasmic Reticulum Stress Pathway.Cancer research communications · 2023Article
- Estrogen-mediated mechanisms in hypertension and other cardiovascular diseases.Journal of human hypertension · 2023Review
- Hypertension after the Menopause: What Can We Learn from Experimental Studies?Physiological research · 2023Review
- The G protein-coupled oestrogen receptor GPER in health and disease: an update.Nature reviews. Endocrinology · 2023Review
- G Protein-Coupled Estrogen Receptor GPER: Molecular Pharmacology and Therapeutic Applications.Annual review of pharmacology and toxicology · 2023Review
- Optogenetic demonstration of the involvement of SMA-negative mural cells in the regulation of cerebral blood flow.Frontiers in physiology · 2023Article
- G protein-coupled estrogen receptor: a promising therapeutic target for aldosterone-induced hypertension.Frontiers in endocrinology · 2023Review
- The emerging role of estrogen's non-nuclear signaling in the cardiovascular disease.Frontiers in cardiovascular medicine · 2023Review
- Sex differences in vascular aging and impact of GPER deletion.American journal of physiology. Heart and circulatory physiology · 2022Article
- G-Protein-Coupled Estrogen Receptor Expression in Rat Uterine Artery Is Increased by Pregnancy and Induces Dilation in a CaInternational journal of molecular sciences · 2022Article
- Assessment of G Protein-Coupled Oestrogen Receptor Expression in Normal and Neoplastic Human Tissues Using a Novel Rabbit Monoclonal Antibody.International journal of molecular sciences · 2022Article
3 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Our previous work showed that chronic activation of the membrane-bound estrogen receptor GPR30/GPER significantly lowers blood pressure in ovariectomized hypertensive mRen2.Lewis female rats which may, in part, reflect direct vasodilatory actions. The current study assessed the hypothesis that cyclic adenosine monophosphate (cAMP) signaling contributes to GPER-mediated vasorelaxation. In mesenteric resistance arteries from intact Lewis females, relaxation to 17-β-estradiol (E2; 47±3% of phenylephrine contraction vs. vehicle 89±2%, P<0.001) or G-1 (44±8%, P<0.001) was blunted to a similar extent by denuding (P<0.001) or the nitric oxide synthase inhibitor l-NAME (P<0.001). In contrast, the cyclooxygenase inhibitor indomethacin did not alter vasodilation (P>0.05). The cAMP analog Rp-cAMPS partially attenuated vasodilation (65±7%, P<0.001), while the combination of l-NAME and Rp-cAMPS exhibited additive effects to effectively abolish vasorelaxation (P>0.05 vs. vehicle). Pretreatment of endothelium-intact vessels with the adenylyl cyclase inhibitor SQ (63±6%) or the guanylyl cyclase inhibitor ODQ (62±9%) both partially inhibited the response to G-1 (P<0.01), while pretreatment with the both inhibitors completely abolished vasorelaxation (P>0.05 vs. vehicle). In denuded vessels only SQ reduced the response (88±3%, P<0.001). Moreover, G-1 significantly increased intracellular cAMP levels in cultured mesenteric smooth muscle cells (P<0.05). We conclude that GPER-dependent vasorelaxation apparently involves both endothelial release of nitric oxide which activates guanylyl cyclase and smooth muscle cell activation of adenylyl cyclase. Downstream production of cyclic nucleotides and stimulation of protein kinases may phosphorylate proteins to promote vascular smooth muscle cell relaxation. The ability of GPER to initiate these signaling pathways may contribute to the beneficial vascular effects of estrogen.
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Registered trials
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.