ArticleExperimental physiology2013
Bradycardic effects mediated by activation of G protein-coupled estrogen receptor in rat nucleus ambiguus.
Article in Experimental physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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16 citing papers in PubMed, 28 citations in OpenAlex.
- Concentration QTc analysis of giredestrant: Overcoming QT/heart rate confounding in the presence of drug-induced heart rate changes.Clinical and translational science · 2023Article
- The G-Protein-Coupled Estrogen Receptor Agonist G-1 Inhibits Proliferation and Causes Apoptosis in Leukemia Cell Lines of T Lineage.Frontiers in cell and developmental biology · 2022Article
- Functional Interaction of Endothelin Receptors in Mediating Natriuresis Evoked by G Protein-Coupled Estrogen Receptor 1.The Journal of pharmacology and experimental therapeutics · 2021Article
- Sex-steroid-dependent plasticity of brain-stem autonomic circuits.American journal of physiology. Regulatory, integrative and comparative physiology · 2020Review
- Adrenergic agonist induces rhythmic firing in quiescent cardiac preganglionic neurons in nucleus ambiguous via activation of intrinsic membrane excitability.Journal of neurophysiology · 2019Article
- Central serotonin and the control of arterial blood pressure and heart rate in infant rats: influence of sleep state and sex.American journal of physiology. Regulatory, integrative and comparative physiology · 2018Article
- Activation of GPER ameliorates experimental pulmonary hypertension in male rats.European journal of pharmaceutical sciences : official journal of the European Federation for Pharmaceutical Sciences · 2017Article
- GPER-novel membrane oestrogen receptor.Clinical science (London, England : 1979) · 2016Review
- G protein-coupled estrogen receptor-mediated effects on cytosolic calcium and nanomechanics in brain microvascular endothelial cells.Journal of neurochemistry · 2015Article
- Evidence for role of acid-sensing ion channels in nucleus ambiguus neurons: essential differences in anesthetized versus awake rats.Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology · 2014Article
- HIV-1-Tat excites cardiac parasympathetic neurons of nucleus ambiguus and triggers prolonged bradycardia in conscious rats.American journal of physiology. Regulatory, integrative and comparative physiology · 2014Article
- Estrogen biology: new insights into GPER function and clinical opportunities.Molecular and cellular endocrinology · 2014Review
- Urotensin II promotes vagal-mediated bradycardia by activating cardiac-projecting parasympathetic neurons of nucleus ambiguus.Journal of neurochemistry · 2014Article
- Nesfatin-1 activates cardiac vagal neurons of nucleus ambiguus and elicits bradycardia in conscious rats.Journal of neurochemistry · 2013Article
- Aldosterone increases cardiac vagal tone via G protein-coupled oestrogen receptor activation.The Journal of physiology · 2013Article
- Differential activation of cultured neonatal cardiomyocytes by plasmalemmal versus intracellular G protein-coupled receptor 55.The Journal of biological chemistry · 2013Article
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5 authors at 5 institutions in 1 country.
Funding
Abstract
The G protein-coupled estrogen receptor (GPER) has been identified in several brain regions, including cholinergic neurons of the nucleus ambiguus, which are critical for parasympathetic cardiac regulation. Using calcium imaging and electrophysiological techniques, microinjection into the nucleus ambiguus and blood pressure measurement, we examined the in vitro and in vivo effects of GPER activation in nucleus ambiguus neurons. A GPER selective agonist, G-1, produced a sustained increase in cytosolic Ca(2+) concentration in a concentration-dependent manner in retrogradely labelled cardiac vagal neurons of nucleus ambiguus. The increase in cytosolic Ca(2+) produced by G-1 was abolished by pretreatment with G36, a GPER antagonist. G-1 depolarized cultured cardiac vagal neurons of the nucleus ambiguus. The excitatory effect of G-1 was also identified by whole-cell visual patch-clamp recordings in nucleus ambiguus neurons, in medullary slices. To validate the physiological relevance of our in vitro studies, we carried out in vivo experiments. Microinjection of G-1 into the nucleus ambiguus elicited a decrease in heart rate; the effect was blocked by prior microinjection of G36. Systemic injection of G-1, in addition to a previously reported decrease in blood pressure, also reduced the heart rate. The G-1-induced bradycardia was prevented by systemic injection of atropine, a muscarinic antagonist, or by bilateral microinjection of G36 into the nucleus ambiguus. Our results indicate that GPER-mediated bradycardia occurs via activation of cardiac parasympathetic neurons of the nucleus ambiguus and support the involvement of the GPER in the modulation of cardiac vagal tone.
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