2016
DOI: 10.1016/j.anl.2015.12.002
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Immunohistochemical localization of alpha and beta adrenergic receptors in the human nasal turbinate

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Cited by 6 publications
(5 citation statements)
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“…The discrepancies in α-ARs’ involvement in the PTGS-2 expression in response to noradrenaline influence in the inflamed endometrium and earlier reports [ 41 , 47 ] can be related to the experimental model (cells, tissue explants) and kind of tissues. Considering the fact that α-ARs are largely located in vascular cells [ 29 , 50 ], the noradrenaline effect found on the PTGS-2 expression (also mPTGES-1 expression, PGE2 secretion) in the E. coli group endometrial explants could be due to changes in blood flow. It should also be added that downstream mechanisms of AR activation are not fully recognized.…”
Section: Discussionmentioning
confidence: 99%
“…The discrepancies in α-ARs’ involvement in the PTGS-2 expression in response to noradrenaline influence in the inflamed endometrium and earlier reports [ 41 , 47 ] can be related to the experimental model (cells, tissue explants) and kind of tissues. Considering the fact that α-ARs are largely located in vascular cells [ 29 , 50 ], the noradrenaline effect found on the PTGS-2 expression (also mPTGES-1 expression, PGE2 secretion) in the E. coli group endometrial explants could be due to changes in blood flow. It should also be added that downstream mechanisms of AR activation are not fully recognized.…”
Section: Discussionmentioning
confidence: 99%
“…Immunohistochemical analysis was carried out using antihuman adrenergic subtype-specific protein antibodies (α1A-, α1D-, α2C-and β2-adrenergic receptors). The immunostaining displayed that submucosal glands contain a high amount of α1D-and β2-adrenergic receptors while smooth muscle surrounding the vasculature contains a high amount of α1A-and α2C-adrenergic receptors (Shirasaki, Kanaizumi, and Himi 2016).…”
Section: Autonomic Receptorsmentioning
confidence: 99%
“…One example is an α-adrenergic receptor agonist drug that mimics sympathetic agents to increase airflow. They function by binding to adrenergic receptors, which starts a excitatory cascade that results in decreased volume of the nasal mucosa, which decreases resistance and increases airflow (Shirasaki, Kanaizumi, and Himi 2016).…”
Section: Airway Resistancementioning
confidence: 99%
“…ARs are cell membrane receptors included in the seven-transmembrane-spanning G-protein coupled receptor (GPCR) superfamily, formed by membrane proteins triggered by extracellular ligands such as small organic molecules, peptides, and neurotransmitters [15]. Structurally, GPCRs are formed by seven hydrophobic transmembrane segments which cross the plasma membrane with an extracellular amino terminus and an intracellular carboxyl-terminus.…”
Section: Introductionmentioning
confidence: 99%
“…According to their pharmacological response, ARs were subdivided into α and β types: these latter types were further divided into three families called β1, β2 and β3 on the basis of molecular classification [19,20]. β2-ARs have been described in multiple locations such as the lung, heart, blood vessels, and nasal turbinates [13,15,20]. However, there is little data available on the presence of β2-ARs in the adrenal gland.…”
Section: Introductionmentioning
confidence: 99%