Abstract
Original language | English |
---|---|
Journal | Frontiers in Physiology |
Volume | 5 |
Issue number | JUL |
DOIs | |
Publication status | Published - 2014 |
Keywords
- Adrenal gland
- Adrenergic system
- Catecholamine
- Functional recovery
- GRK2
- Heart failure
- β-adrenergic receptor
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In: Frontiers in Physiology, Vol. 5 , No. JUL, 2014.
Research output: Contribution to journal › Article › peer-review
TY - JOUR
T1 - Adrenal adrenoceptors in heart failure
AU - de Lucia, C.
AU - Femminella, G.D.
AU - Gambino, G.
AU - Pagano, G.
AU - Allocca, E.
AU - Rengo, C.
AU - Silvestri, C.
AU - Leosco, D.
AU - Ferrara, N.
AU - Rengo, G.
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PY - 2014
Y1 - 2014
N2 - 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): a2ARs 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 a2AR 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 a2AR 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. © 2014 de Lucia, Femminella, Gambino, Pagano, Allocca, Rengo, Silvestri, Leosco, Ferrara and Rengo.
AB - 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): a2ARs 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 a2AR 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 a2AR 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. © 2014 de Lucia, Femminella, Gambino, Pagano, Allocca, Rengo, Silvestri, Leosco, Ferrara and Rengo.
KW - Adrenal gland
KW - Adrenergic system
KW - Catecholamine
KW - Functional recovery
KW - GRK2
KW - Heart failure
KW - β-adrenergic receptor
UR - https://www.scopus.com/inward/record.uri?eid=2-s2.0-84904307770&partnerID=40&md5=d23f1b05a2919c8f2430224d7e79fcf5
U2 - 10.3389/fphys.2014.00246
DO - 10.3389/fphys.2014.00246
M3 - Article
SN - 1664-042X
VL - 5
JO - Frontiers in Physiology
JF - Frontiers in Physiology
IS - JUL
ER -