ArticleFrontiers in neurology2014
β1-Blockers Lower Norepinephrine Release by Inhibiting Presynaptic, Facilitating β1-Adrenoceptors in Normotensive and Hypertensive Rats.
Article in Frontiers in neurology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 37 citations in OpenAlex.
- Neuroprotective actions of norepinephrine in neurological diseases.Pflugers Archiv : European journal of physiology · 2024Review
- Beta-Blockers and Their Current Role in Maternal and Neonatal Health: A Narrative Review of the Literature.Cureus · 2023Review
- Neuroprotective Effect of Platinum Nanoparticles Is Not Associated with Their Accumulation in the Brain of Rats.Journal of functional biomaterials · 2023Article
- Increased Renal Dysfunction, Apoptosis, and Fibrogenesis Through Sympathetic Hyperactivity After Focal Cerebral Infarction.Translational stroke research · 2022Article
- Cardiac sympathetic activation circumvents high-dose beta blocker therapy in part through release of neuropeptide Y.JCI insight · 2020Article
- Effects of βBMC pharmacology & toxicology · 2020Article
- Chronic Testosterone Increases Impulsivity and Influences the Transcriptional Activity of the Alpha-2A Adrenergic Receptor Signaling Pathway in Rat Brain.Molecular neurobiology · 2019Article
- Dose-independent influence of metoprolol on cardiac and motor functions, QoL, and mental status in Chinese patients with CHF.Therapeutics and clinical risk management · 2019Article
- Comparison of clinical efficacy of metoprolol combined with irbesartan and hydrochlorothiazide and non-invasive ventilator in the emergency treatment of patients with severe heart failure.Experimental and therapeutic medicine · 2018Article
- Neurotransmitter Switching Coupled to β-Adrenergic Signaling in Sympathetic Neurons in Prehypertensive States.Hypertension (Dallas, Tex. : 1979) · 2018Article
- Kv7(KCNQ)-KFrontiers in physiology · 2018Article
- Adrenergic Blockade Bi-directionally and Asymmetrically Alters Functional Brain-Heart Communication and Prolongs Electrical Activities of the Brain and Heart during Asphyxic Cardiac Arrest.Frontiers in physiology · 2018Article
- Stroke-induced chronic systolic dysfunction driven by sympathetic overactivity.Annals of neurology · 2017Article
- β- and αFrontiers in neurology · 2017Article
- Voltage-Sensitive K(+) Channels Inhibit Parasympathetic Ganglion Transmission and Vagal Control of Heart Rate in Hypertensive Rats.Frontiers in neurology · 2015Article
- Altered β1-3-adrenoceptor influence on α2-adrenoceptor-mediated control of catecholamine release and vascular tension in hypertensive rats.Frontiers in physiology · 2015Article
- β3-adrenoceptors inhibit stimulated norepinephrine release in spontaneously hypertensive rats.Frontiers in physiology · 2014Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Peripheral norepinephrine release is facilitated by presynaptic β-adrenoceptors, believed to involve the β2-subtype exclusively. However, β1-selective blockers are the most commonly used β-blockers in hypertension. Here the author tested the hypothesis that β1AR may function as presynaptic, release-facilitating auto-receptors. Since β1AR-blockers are injected during myocardial infarction, their influence on the cardiovascular response to acute norepinephrine release was also studied. By a newly established method, using tyramine-stimulated release through the norepinephrine transporter (NET), presynaptic control of catecholamine release was studied in normotensive and spontaneously hypertensive rats. β1AR-selective antagonists (CGP20712A, atenolol, metoprolol) reduced norepinephrine overflow to plasma equally efficient as β2AR-selective (ICI-118551) and β1+2AR (nadolol) antagonists in both strains. Neither antagonist lowered epinephrine secretion. Atenolol, which does not cross the blood-brain barrier, reduced norepinephrine overflow after adrenalectomy (AdrX), AdrX + ganglion blockade, losartan, or nephrectomy. Atenolol and metoprolol reduced resting cardiac work load. During tyramine-stimulated norepinephrine release, they had little effect on work load, and increased the transient rise in total peripheral vascular resistance, particularly atenolol when combined with losartan. In conclusion, β1AR, like β2AR, stimulated norepinephrine but not epinephrine release, independent of adrenal catecholamines, ganglion transmission, or renal renin release/angiotensin AT1 receptor activation. β1AR therefore functioned as a peripheral, presynaptic, facilitating auto-receptor. Like tyramine, hypoxia may induce NET-mediated release. Augmented tyramine-induced vasoconstriction, as observed after injection of β1AR-blocker, particularly atenolol combined with losartan, may hamper organ perfusion, and may have clinical relevance in hypoxic conditions such as myocardial infarction.
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