ReviewFrontiers in physiology2014
Adrenal adrenoceptors in heart failure.
Review in Frontiers in physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
24 citing papers in PubMed, 49 citations in OpenAlex.
- β-Adrenergic Receptors: Not Always Outside-In.Physiology (Bethesda, Md.) · 2026Review
- Adrenoceptor Desensitization: Current Understanding of Mechanisms.Pharmacological reviews · 2024Review
- CardiOmics signatures reveal therapeutically actionable targets and drugs for cardiovascular diseases.Heliyon · 2024Article
- The βAdvances in pharmacological and pharmaceutical sciences · 2024Review
- Heart-brain interaction in cardiogenic dementia: pathophysiology and therapeutic potential.Frontiers in cardiovascular medicine · 2024Review
- Controls of Central and Peripheral Blood Pressure and Hemorrhagic/Hypovolemic Shock.Journal of clinical medicine · 2023Review
- Role of β-blockers in Preventing Heart Failure and Major Adverse Cardiac Events Post Myocardial Infarction.Current cardiology reviews · 2023Review
- The effects of perioperative dexmedetomidine infusion on hemodynamic stability during laparoscopic adrenalectomy for pheochromocytoma: a randomized study.Frontiers in medicine · 2023Article
- Review
- Review
- β-Adrenergic receptor, an essential target in cardiovascular diseases.Heart failure reviews · 2020Review
- High-dose nitrate therapy recovers the expression of subtypes αBMC cardiovascular disorders · 2020Article
- Catestatin reverses the hypertrophic effects of norepinephrine in H9c2 cardiac myoblasts by modulating the adrenergic signaling.Molecular and cellular biochemistry · 2020Article
- Slow breathing improves cardiovascular reactivity to mental stress and health-related quality of life in heart failure patients with reduced ejection fraction.Cardiology journal · 2020Article
- Long-Term Caloric Restriction Improves Cardiac Function, Remodeling, Adrenergic Responsiveness, and Sympathetic Innervation in a Model of Postischemic Heart Failure.Circulation. Heart failure · 2018Article
- New Insights in Cardiac β-Adrenergic Signaling During Heart Failure and Aging.Frontiers in pharmacology · 2018Review
- Alpha2-adrenoceptors in adrenomedullary chromaffin cells: functional role and pathophysiological implications.Pflugers Archiv : European journal of physiology · 2018Review
- Targeting GPCR-Gβγ-GRK2 signaling as a novel strategy for treating cardiorenal pathologies.Biochimica et biophysica acta. Molecular basis of disease · 2017Review
- microRNA in Cardiovascular Aging and Age-Related Cardiovascular Diseases.Frontiers in medicine · 2017Review
- Easy-to-use strategy for reference gene selection in quantitative real-time PCR experiments.Naunyn-Schmiedeberg's archives of pharmacology · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Heart failure (HF) is a chronic clinical syndrome characterized by the reduction in left ventricular (LV) function and it represents one of the most important causes of morbidity and mortality worldwide. Despite considerable advances in pharmacological treatment, HF represents a severe clinical and social burden. Sympathetic outflow, characterized by increased circulating catecholamines (CA) biosynthesis and secretion, is peculiar in HF and sympatholytic treatments (as β-blockers) are presently being used for the treatment of this disease. Adrenal gland secretes Epinephrine (80%) and Norepinephrine (20%) in response to acetylcholine stimulation of nicotinic cholinergic receptors on the chromaffin cell membranes. This process is regulated by adrenergic receptors (ARs): α2ARs inhibit CA release through coupling to inhibitory Gi-proteins, and β ARs (mainly β2ARs) stimulate CA release through coupling to stimulatory Gs-proteins. All ARs are G-protein-coupled receptors (GPCRs) and GPCR kinases (GRKs) regulate their signaling and function. Adrenal GRK2-mediated α2AR desensitization and downregulation are increased in HF and seem to be a fundamental regulator of CA secretion from the adrenal gland. Consequently, restoration of adrenal α2AR signaling through the inhibition of GRK2 is a fascinating sympatholytic therapeutic strategy for chronic HF. This strategy could have several significant advantages over existing HF pharmacotherapies minimizing side-effects on extra-cardiac tissues and reducing the chronic activation of the renin-angiotensin-aldosterone and endothelin systems. The role of adrenal ARs in regulation of sympathetic hyperactivity opens interesting perspectives in understanding HF pathophysiology and in the identification of new therapeutic targets.
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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.