Regulation of catecholamine release in human adrenal chromaffin cells by β-adrenoceptors

Cortez, Vera; Santana, Magda M.; Marques, Ana Patrícia; Mota, A.; Rosmaninho‐Salgado, Joana; Cavadas, Cláudia

doi:10.1016/j.neuint.2011.12.018

Cited by 26 publications

(16 citation statements)

References 45 publications

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“…Yet another hypoglycaemic effect attributed to β 3 ARs, albeit indirectly, is the vasodilatory effects on WAT and pancreatic islet vasculature, which was confirmed through the use of the selective β 3 AR antagonist (SR‐59230A) in the Goto‐Kakizaki rat (a mildly obese type 2 DM model) . As previously stated, β 3 ARs also stimulate the secretion of basal and evoked E and NE release in human adrenal chromaffin cells , which may further complicate existing impairments on glucose metabolism.…”

Section: β3 Arsmentioning

confidence: 67%

Peripheral Adrenoceptors: The Impetus Behind Glucose Dysregulation and Insulin Resistance

Boyda

Procyshyn

Pang

et al. 2013

J Neuroendocrinology

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It is now accepted that several pharmacological drug treatments trigger clinical manifestations of glucose dysregulation, such as hyperglycaemia, glucose intolerance and insulin resistance, in part through poorly understood mechanisms. Persistent sympathoadrenal activation is linked to glucose dysregulation and insulin resistance, both of which significantly increase the risk of emergent endocrinological disorders, including metabolic syndrome and type 2 diabetes mellitus. Through the use of targeted mutagenesis and pharmacological methods, preclinical and clinical research has confirmed physiological glucoregulatory roles for several peripheral a-and b-adrenoceptor subtypes. Adrenoceptor isoforms in the pancreas (a 2A and b 2 ), skeletal muscle (a 1A and b 2 ), liver (a 1A & B and b 2 ) and adipose tissue (a 1A and b 1 & 3 ) are convincing aetiological targets that account for both immediate and long-lasting alterations in blood glucose homeostasis. Because significant overlap exists between the therapeutic applications of numerous classes of drugs and their associated adverse side-effects, a better understanding of peripheral adrenoceptor-mediated glucose metabolism is thus warranted. Therefore, at the same time as providing a brief review of glucose homeostasis in the periphery, the present review addresses both functional and pathophysiological roles of the mammalian a 1 , a 2 , and b-adrenoceptor isoforms in whole-body glucose turnover. We highlight evidence relating to the clinical use of common adrenergic drugs and their impacts on glucose metabolism.

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Section: β3 Arsmentioning

confidence: 67%

Peripheral Adrenoceptors: The Impetus Behind Glucose Dysregulation and Insulin Resistance

Boyda

Procyshyn

Pang

et al. 2013

J Neuroendocrinology

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“…20 To clarify the manner by which these stress-related biobehavioral factors accelerate the progression of periodontitis, a further analysis of the AR levels was performed. The α1-AR and β2-receptor (β2-AR) are generally considered to be involved in brain-immune communication.…”

Section: Resultsmentioning

confidence: 99%

Chronic stress enhances progression of periodontitis via α1-adrenergic signaling: a potential target for periodontal disease therapy

Wang

et al. 2014

Exp Mol Med

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This study assessed the roles of chronic stress (CS) in the stimulation of the sympathetic nervous system and explored the underlying mechanisms of periodontitis. Using an animal model of periodontitis and CS, the expression of tyrosine hydroxylase (TH) and the protein levels of the α1-adrenergic receptor (α1-AR) and β2-adrenergic receptor (β2-AR) were assessed. Furthermore, human periodontal ligament fibroblasts (HPDLFs) were stimulated with lipopolysaccharide (LPS) to mimic the process of inflammation. The proliferation of the HPDLFs and the expression of α1-AR and β2-AR were assessed. The inflammatory-related cytokines interleukin (IL)-1β, IL-6 and IL-8 were detected after pretreatment with the α1/β2-AR blockers phentolamine/propranolol, both in vitro and in vivo. Results show that periodontitis under CS conditions enhanced the expression of TH, α1-AR and β2-AR. Phentolamine significantly reduced the inflammatory cytokine levels. Furthermore, we observed a marked decrease in HPDLF proliferation and the increased expression of α1-ARfollowing LPS pretreatment. Pretreatment with phentolamine dramatically ameliorated LPS-inhibited cell proliferation. In addition, the blocking of α1-ARsignaling also hindered the upregulation of the inflammatory-related cytokines IL-1β, IL-6 and IL-8. These results suggest that CS can significantly enhance the pathological progression of periodontitis by an α1-adrenergic signaling-mediated inflammatory response. We have identified a potential therapeutic target for the treatment of periodontal disease, particularly in those patients suffering from concurrent CS.

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“…Nevertheless, an increase in adrenal medulla size induced by chronic stress is often associated with increases in expression, synthesis and activity of catecholamine biosynthetic enzymes [see Kvetnansky et al (2009) for review]. Moreover, increased neurosecretory capacity and/or more efficient storage, through changes in NPY, CgA and catecholamine transporter levels, have also been suggested as an important response of adrenal medulla to repeated exposure to stress (Cavadas et al, 2006(Cavadas et al, , 2001Cortez et al, 2012;Rosmaninho-Salgado et al, 2007, 2009Sabban et al, 2012;Tillinger et al, 2010). The alterations we observed in adrenal medullary catecholaminergic system after 7 days of UCS (increased TH, DβH, PNMT, NPY, SNAP25 and VMAT2 mRNA and/or protein) also indicates that adrenal medulla initially responds by enhancing the capacity of chromaffin cells to synthesize, store and release catecholamines.…”

Section: Npymentioning

confidence: 99%

Impaired adrenal medullary function in a mouse model of depression induced by unpredictable chronic stress

Santana

Rosmaninho‐Salgado

Cortez

et al. 2015

European Neuropsychopharmacology

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Regulation of catecholamine release in human adrenal chromaffin cells by β-adrenoceptors

Cited by 26 publications

References 45 publications

Peripheral Adrenoceptors: The Impetus Behind Glucose Dysregulation and Insulin Resistance

Peripheral Adrenoceptors: The Impetus Behind Glucose Dysregulation and Insulin Resistance

Chronic stress enhances progression of periodontitis via α1-adrenergic signaling: a potential target for periodontal disease therapy

Impaired adrenal medullary function in a mouse model of depression induced by unpredictable chronic stress

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