Disease relevance of Adrb1

• T3 replacement reversed the changes in cardiac responses and metabolic parameters, except body weight, but produced cardiac symptoms of hyperthyroidism (tachycardia, hypertrophy as well as an increased beta 1-adrenoceptor density) [1].
• We conclude that neonatal hypothyroidism produces pronounced physiological responses, changes in adrenoceptor-mediated responses and an increased ventricular beta 1-adrenoceptor density [1].
• In contrast, a major component of the beta 1-adrenoceptor mediated tachycardia produced by dopamine in guinea pig atria was indirect in nature as evidenced by the marked attenuation in potency that occurred following catecholamine depletion with reserpine [2].
• CONCLUSION: In the infarcted myocardium total beta-adrenoceptor density is decreased due to a decreased beta1-adrenoceptor density at 12 weeks after myocardial infarction [3].
• Neither dobutamine nor prenalterol, which are beta-1 adrenoceptor agonists and like DPX, potent chronotropic and inotropic agents were effective in preventing OFR induced lethal toxicity [4].

High impact information on Adrb1

• Predominant expression of beta 1-adrenergic receptor in the thick ascending limb of rat kidney. Absolute mRNA quantitation by reverse transcription and polymerase chain reaction [5].
• Displacement of specific binding by the beta 1-adrenoceptor antagonist pafenolol and the beta 2-adrenoceptor antagonist ICI 118.551 revealed that the colon preparation possessed a heterogenous beta-adrenoceptor population [6].
• Chronic hypoxia increases beta 1-adrenergic receptor mRNA and density but not signaling in neonatal rat cardiac myocytes [7].
• Isoproterenol (1 mumol/L) and denopamine (10 mumol/L) mimicked the effects of NE, but phenylephrine did not, indicating that NE-induced microtubular disassembly is mediated by beta 1-adrenergic receptor stimulation [8].
• Cardiac beta 1-adrenoceptor blockade with metoprolol abolished the tachycardic and reduced the pressor responses [9].

Chemical compound and disease context of Adrb1

• Terbutaline (an agonist of beta2-adrenoceptor) and dobutamine (an agonist of beta1-adrenoceptor), both are able to increase intracellular cAMP via activation of adenylate cyclase, were examined in the anesthetized rat with endotoxemia [10].
• Instead, the inhibition by urapidil of stimulation-evoked tachycardia could be accounted for by its beta 1-adrenoreceptor antagonistic effect [11].
• Protein kinase C-mediated down-regulation of beta1-adrenergic receptor gene expression in rat C6 glioma cells [12].
• Agonist and cyclic AMP-mediated regulation of beta 1-adrenergic receptor mRNA and gene transcription in rat C6 glioma cells [13].
• 5. Treatment with the beta 1-adrenoceptor antagonist, atenolol, in a dose of 80 mg kg-1 body weight abolished right ventricular hypertrophy in response to 7% inspired oxygen, without affecting haematocrit and caused a small reduction in the ratio of heart weight to body weight in normoxic rats [14].

Biological context of Adrb1

• The selective beta 1 adrenoceptor antagonist CGP20712A (100 nmol.litre-1) displaced about 30% and 50% of the total atrioventricular node binding sites in diabetic and control hearts, respectively [15].
• The effects of the beta 1-adrenoceptor blocking drug atenolol and the beta 2-adrenoceptor blocking drug ICI 118551 (ICI, Melbourne, Australia) on noradrenaline release and blood pressure were investigated using the pithed rat, which was subjected to continuous electrical stimulation of the spinal sympathetic outflow (pulses at 3 Hz) [16].
• Colchicine pretreatment completely inhibited (-)-isoproterenol-induced down-regulation of beta 1-adrenergic receptor mRNA, but not that of beta 2-adrenergic receptor mRNA [17].
• 6. The beta3-adrenoceptor antagonist SR 59230A (which, by itself, caused a beta1-adrenoceptor-mediated increase in heart rate and, for this reason, was studied after administration of a low dose of CGP 20712) attenuated the cardiostimulant and the thermogenic effect of CGP 12177 to a similar extent [18].
• PKA-mediated phosphorylation of the beta1-adrenergic receptor promotes Gs/Gi switching [19].

Anatomical context of Adrb1

• Thyroid hormones transcriptionally regulate the beta 1-adrenergic receptor gene in cultured ventricular myocytes [20].
• Immunoblots of membranes prepared from myocytes revealed a marked increase by T3 in the 64-kDa species of the beta 1-adrenergic receptor [20].
• These studies indicate that thyroid hormones regulate the cardiac beta-adrenergic receptor-adenylate cyclase system by controlling the rate of transcription of the beta 1-adrenergic receptor gene [20].
• We conclude that NA depolarizes striatal cholinergic interneurons via beta1-adrenoceptor activation, through a cAMP-dependent but PKA-independent mechanism [21].
• The mammalian beta 1-adrenergic receptor of rat fat cells has also been purified (Cubero, A., and Malbon, C.C. (1984) J. Biol. Chem. 259, 1344-1350) [22].

Associations of Adrb1 with chemical compounds

• The rate of beta 1-adrenergic receptor gene transcription assessed by nuclear run-on transcription assays increased by 3.4 +/- 0.4-fold in cells treated for 30 min with T3 [20].
• A tenet of beta1-adrenergic receptor (beta1AR) signaling is that stimulation of the receptor activates the adenylate cyclase-cAMP-protein kinase A (PKA) pathway, resulting in positive inotropic and relaxant effects in the heart [23].
• Atenolol (beta 1-adrenoceptor antagonist) had no effect on the renal responses to air stress when given alone or before isoproterenol [24].
• In contrast, intracerebroventricular administration of the beta 1-adrenergic receptor antagonist atenolol (30 micrograms) had no effect on the renal responses to air stress [25].
• Pretreatment of 8-day-old rats with 5 mg/kg CGP 20712A (a selective beta 1-adrenergic receptor antagonist) did not change the plasma ACTH response to insulin injection, while pretreatment with 2.5 mg/kg ICI 118551 (a selective beta 2-adrenergic receptor antagonist) resulted in a significant decrease of the IIH-induced stimulation of ACTH secretion [26].

Regulatory relationships of Adrb1

• Evidence that beta 1-adrenoceptor activation mediates isoproterenol-stimulated renin secretion in the rat [27].

Other interactions of Adrb1

• Finally, double-labeling experiments combining beta1-adrenoceptor and choline acetyltransferase immunocytochemistry by means of confocal microscopy revealed a strong beta1-adrenoceptor labeling on cholinergic interneurons [21].
• In addition, the results indicated that DA attenuation of iNOS was significantly impeded by the adenylate cyclase inhibitor MDL-12,330A, the D(1) antagonist SCH-23390, the beta2 adrenergic receptor antagonist ICI-118,551 and the beta1 adrenergic receptor antagonist atenolol [28].
• On the other hand, neither the selective beta 1-adrenoceptor antagonist, betaxolol, the selective beta 2-adrenoceptor antagonist, ICI 118.551, nor the 5-HT2 receptor antagonist, ketanserin, affected 8-OH-DPAT-induced increases in plasma adrenaline levels [29].
• In contrast, endothelin-1-induced effects were increased (p<0.05) by microinjections into the superior colliculus of prazosin (2.4 nmol) (49 +/- 7%, n=5), an alpha1-adrenoceptor antagonist; dobutamine (4 nmol) (51 +/- 9%, n=5), a beta1-adrenoceptor agonist or isoprenaline (1 nmol) (49 +/- 6%, n=5), a beta1/beta2-adrenoceptor agonist [30].
• Conversely, pressor overactivity of AngII was observed in the anterior hypothalamic area of ACo rats at a chronic hypertensive stage; this enhancement could be explained, at least in part, by the pressor beta1-adrenoceptor activity [31].

Analytical, diagnostic and therapeutic context of Adrb1

• Northern blot hybridization also showed a rapid and sustained increase of 2.2 +/- 0.4-fold (n = 4) in beta 1-adrenergic receptor mRNA [20].
• In contrast, PVN microinjections of both the beta 1 adrenoceptor agonist dobutamine and the beta 2 adrenoceptor agonist salbutamol significantly reduced basal plasma AVP [32].
• The result of the present study demonstrate that the usual dominance of the beta 1-adrenoceptor subtype in eliciting amylase release is lost, implying that the differentiation of the beta-adrenoceptor into its subtypes is altered by neonatal sympathetic denervation [33].
• The beta 1-adrenergic receptor of rat fat cells was effectively solubilized with digitonin and purified by affinity chromatography and steric exclusion high pressure liquid chromatography (HPLC) [34].
• Metabolic labelling of cells with [35S]-methionine in tandem with immunoprecipitation by beta 1-adrenergic-receptor-specific antibodies reveals a sharp decline in the synthesis of the receptor within 48 h for cells challenged with glucocorticoid [35].

References