Responsiveness, affinity constants and <sub>2</sub>‐adrenoceptor reserves for isoprenaline on portal veins from normo‐ and pre‐ and hypertensive rats

Chen, Y.‐Y.; Doggrell, Sheila A

doi:10.1046/j.1474-8673.2003.00275.x

Cited by 1 publication

(1 citation statement)

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“…Bromoacetylalprenololmenthan (BAAM), a strong alkylating irreversible antagonist of the βadrenergic receptor [24], was used to examine the inhibition and regeneration of β-adrenergic receptor after lung radiation. In the antagonist group (n = 25), rats received a single subcutaneous injection of BAAM (Sigma-Aldrich) at a dose level of 50 mg/kg.…”

Section: In Vivo Inhibition Of β-Adrenergic Receptormentioning

confidence: 99%

Modulation of β-adrenergic receptor in rat lung after gamma irradiation

Qiang

Liao

Zhang

et al. 2014

Journal of X-Ray Science and Technology

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OBJECTIVES: To study the effect of γ irradiation on β-adrenergic receptors of the lung. MATERIALS AND METHODS: Healthy Sprague-Dawley rats were used as an animal model. Cell membrane proteins of lung tissue were harvested after the whole lung received 20 Gy of 60 Co γ irradiation. 125 I-labeled iodopindolol ( 125 I-IPIN) was used as a ligand of β-adrenergic receptors. The numbers of the β-adrenergic receptors were determined by radioligandreceptor binding assay (RBA). Data were compared with irreversible blockage using antagonist bromoacetylalprenololmenthan (BAAM). RESULTS: The post-radiation RBA assay showed that the number of β-adrenergic receptors in lung tissue decreased at a steady rate. It decreased to 48% of the normal level at the 15 th day after irradiation. At 40 days after radiation the level of β-adrenergic receptors started to increase at a steady rate and reached to the normal level around 70 days after radiation. There were significant differences in receptor synthesis, degradation and regeneration rates between irradiation group and BAMM group. CONCLUSIONS: The whole lung irradiation could severely affect the levels of β-adrenergic receptors. The potential clinical implications of radiation-induced changes of β-adrenergic receptors warrant further investigation.These changes are associated with pneumonitis and pulmonary fibrosis although the mechanisms that underlie their pathogenesis are still unclear. Studies suggest that radiation-induced modulation of cellular proteins in various cell organelles might be responsible for the pathogenesis of lung injury [6].A receptor is a protein molecule embedded in either the plasma membrane or cytoplasm of a cell that binds with signaling molecules (i.e. ligand) such as hormones, antigens or drugs. Early studies demonstrate that ionizing radiation has a strong impact on a wide range of receptors that include steroid receptor [7-9], opioid receptor [10], epidermal growth factor receptor (EGFR) and vascular endothelial growth factor (VEGF) receptors [11,12]. The adrenergic receptors (or adrenoreceptors) possessed by many cells are a class of G protein-coupled receptors (GPCRs) that are the targets of catecholamines. Adrenergic signaling is involved in regulating multiple cellular processes that contribute to cancer growth [13]. Early studies show that thoracic radiation can affect the cardiac adrenergic receptors which play significant roles in radiation-induced heart diseases [14][15][16].The stimulation or blockade of lung β-adrenoreceptors has various effects on physiological functions of the lung [17][18][19][20]. In line with this, corticosteroids and adrenoreceptor agonists have been used for the management of various lung diseases including radiation pneumonitis [21,22]. However, to date, the effect of radiation on β-adrenoreceptors in the lung tissues has not been fully explored. The aim of this in vivo study was to utilize a specific receptor-ligand binding assay (RBA) to examine the effect of 60 Co γ irradiation on the levels of β-adrenergic recepto...

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Section: In Vivo Inhibition Of β-Adrenergic Receptormentioning

confidence: 99%