Regulation of the Norepinephrine Transporter by Endothelins

Vatta, Marcelo S.; Bianciotti, Liliana G.; Guil, M.; Hope, Sandra

doi:10.1016/bs.vh.2014.12.013

Cited by 3 publications

(4 citation statements)

References 239 publications

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“…However, Callado and Stamford (2000) were unable to detect an influence on endogenous NE clearance assessed by fast cyclic voltammetry of the a2 antagonist BRL 4408 (2-[2H-(1-methyl-1,3-dihydroisoindole) methyl]-4,5-dihydroimidazole) was applied to locus ceruleus brain slices. With respect to heteroreceptors, Hope and colleagues obtained evidence for cAMP-dependent modulation of NE uptake in hypothalamic preparations downstream of endothelin 1 and 3 receptors (Hope et al, 2008(Hope et al, , 2010Vatta et al, 2015), effects likely mediated by changes in NET trafficking. These receptors however do not couple directly to cAMP production, and thus the cAMP dependence of effects are likely indirect.…”

Section: B Regulation Of Norepinephrine Transport By Proteinmentioning

confidence: 99%

Kinase-dependent Regulation of Monoamine Neurotransmitter Transporters

Bermingham

Blakely

2016

Pharmacol Rev

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Section: B Regulation Of Norepinephrine Transport By Proteinmentioning

confidence: 99%

Kinase-dependent Regulation of Monoamine Neurotransmitter Transporters

Bermingham

Blakely

2016

Pharmacol Rev

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“…In cultured rat neuroblastoma cells (PC12 cell line), exogenous norepinephrine significantly reduces the expression of NET protein but not NET mRNA [ 189 , 190 ], which suggests post-transcriptional downregulation for NET in HF [ 82 ]. Normally, NET located in the cell membrane is regulated by glycosylation [ 191 ]. Therefore, the effect of norepinephrine on the reduction in the neuronal NET density in HF could be associated with endoplasmic reticulum stress-reduced glycosylation, causing the trafficking of NET to the cell membrane [ 190 ].…”

Section: Mechanisms Underlying the Remodeling Of Cardiac Postganglion...mentioning

confidence: 99%

“…Therefore, the effect of norepinephrine on the reduction in the neuronal NET density in HF could be associated with endoplasmic reticulum stress-reduced glycosylation, causing the trafficking of NET to the cell membrane [ 190 ]. Additionally, endothelin binding with endothelin receptors also inhibits NET activity in HF by affecting NET phosphorylation because the NET activity is, in the short and long term, modulated by protein kinase A, C, and G and calcium-calmodulin-dependent protein kinase [ 191 , 192 ]. It is unclear whether NET activity and expression are modulated by other endogenous factors in HF, such as the renin-angiotensin-aldosterone system, bradykinin, nitric oxide, natriuretic peptides, etc.…”

Section: Mechanisms Underlying the Remodeling Of Cardiac Postganglion...mentioning

confidence: 99%

Stellate Ganglia and Cardiac Sympathetic Overactivation in Heart Failure

2022

IJMS

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Heart failure (HF) is a major public health problem worldwide, especially coronary heart disease (myocardial infarction)-induced HF with reduced ejection fraction (HFrEF), which accounts for over 50% of all HF cases. An estimated 6 million American adults have HF. As a major feature of HF, cardiac sympathetic overactivation triggers arrhythmias and sudden cardiac death, which accounts for nearly 50–60% of mortality in HF patients. Regulation of cardiac sympathetic activation is highly integrated by the regulatory circuitry at multiple levels, including afferent, central, and efferent components of the sympathetic nervous system. Much evidence, from other investigators and us, has confirmed the afferent and central neural mechanisms causing sympathoexcitation in HF. The stellate ganglion is a peripheral sympathetic ganglion formed by the fusion of the 7th cervical and 1st thoracic sympathetic ganglion. As the efferent component of the sympathetic nervous system, cardiac postganglionic sympathetic neurons located in stellate ganglia provide local neural coordination independent of higher brain centers. Structural and functional impairments of cardiac postganglionic sympathetic neurons can be involved in cardiac sympathetic overactivation in HF because normally, many effects of the cardiac sympathetic nervous system on cardiac function are mediated via neurotransmitters (e.g., norepinephrine) released from cardiac postganglionic sympathetic neurons innervating the heart. This review provides an overview of cardiac sympathetic remodeling in stellate ganglia and potential mechanisms and the role of cardiac sympathetic remodeling in cardiac sympathetic overactivation and arrhythmias in HF. Targeting cardiac sympathetic remodeling in stellate ganglia could be a therapeutic strategy against malignant cardiac arrhythmias in HF.

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“…Several neuropeptides, including ET-1, regulate a wide variety of biological effects, including noradrenergic transmission and in particular neuronal NE uptake. A recent review discusses the role for the interaction between ET-1 and NE in maintaining neurotransmission homeostasis, further suggesting that this interaction may represent a potential therapeutic target for various diseases, particularly hypertension (Vatta et al 2015). This possibility is supported by the fact that ETA and ETB receptors are implicated in the mediation of contractile responses evoked by NE (Enouri et al 2013).…”

Section: Vascular Nervesmentioning

confidence: 99%

Endothelin-1, endothelin receptor antagonists, and vein graft occlusion in coronary artery bypass surgery: 20 years on and still no journey from bench to bedside

Dashwood

Loesch

2020

Can. J. Physiol. Pharmacol.

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The saphenous vein is the most commonly used bypass graft in patients with coronary artery disease. During routine coronary artery bypass grafting the vascular damage inflicted on the vein is likely to stimulate the release of endothelin-1, a potent endothelium-derived vasoconstrictor that also possesses cell proliferation and inflammatory properties, conditions associated with vein graft failure. In both in vitro and in vivo studies, endothelin receptor antagonists reduce neointimal thickening. The mechanisms underlying these observations are multi-factorial and include an effect on cell proliferation and cell/tissue damage. Much of the data supporting the beneficial action of endothelin-1 receptor antagonism at reducing intimal thickening and occlusion in experimental vein grafts was published over 20 years ago. The theme of the recent ET-16 conference in Kobe was “Visiting Old and Learning New”. This short review article provides an overview of studies showing the potential of endothelin receptor antagonists to offer an adjuvant therapeutic approach for reducing saphenous vein graft failure and poses the question why this important area of research has not been translated from bench to bedside given the potential benefit for coronary artery bypass patients?

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Regulation of the Norepinephrine Transporter by Endothelins

Cited by 3 publications

References 239 publications

Kinase-dependent Regulation of Monoamine Neurotransmitter Transporters

Kinase-dependent Regulation of Monoamine Neurotransmitter Transporters

Stellate Ganglia and Cardiac Sympathetic Overactivation in Heart Failure

Endothelin-1, endothelin receptor antagonists, and vein graft occlusion in coronary artery bypass surgery: 20 years on and still no journey from bench to bedside

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