PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 15494206-1 2005 The cardiac actions of catecholamines have long been attributed to the predominant beta(1)-AR subtype that couples to the classical Gs/AC/cAMP pathway. Catecholamines 23-37 adrenoceptor beta 1 Homo sapiens 83-93 15564877-0 2004 The Arg389Gly beta1-adrenoceptor gene polymorphism determines contractile response to catecholamines. Catecholamines 86-100 adrenoceptor beta 1 Homo sapiens 14-32 15564877-11 2004 CONCLUSION: These data indicate that the Arg389Gly beta1AR polymorphism is functionally relevant in vivo and determines contractile responsiveness to catecholamines in humans. Catecholamines 150-164 adrenoceptor beta 1 Homo sapiens 51-58 15276011-1 2004 The traditional notion that catecholamine actions are mediated by the predominant beta(1)-adrenergic receptor (beta(1)-AR) subtype linked to the activation of adenylyl cyclase and the accumulation of cyclic adenosine 3",5"-monophosphate (cAMP) in cardiomyocytes has been challenged by recent studies showing that cardiomyocytes co-express pharmacologically distinct beta(2)-AR subtypes that activate a more broad range of downstream effectors. Catecholamines 28-41 adrenoceptor beta 1 Homo sapiens 82-121 12439640-20 2002 Both, permanent stimulation with catecholamines and chronic treatment with agonistic anti-beta1-adrenoceptor autoantibodies cause a reduction of the expression of the beta1-adrenoceptor on mRNA and protein level in "in vitro" experiments. Catecholamines 33-47 adrenoceptor beta 1 Homo sapiens 167-185 14608456-13 2003 In contrast, (-)-pindolol blocks the effects of catecholamines through a high-affinity site of the beta(1)-adrenoceptor. Catecholamines 48-62 adrenoceptor beta 1 Homo sapiens 99-119 11809863-1 2002 The beta(1)-adrenergic receptor (beta(1)-AR) plays a key role in regulating heart rate and contractility in response to catecholamines. Catecholamines 120-134 adrenoceptor beta 1 Homo sapiens 4-43 12034720-1 2002 The beta(1)-adrenergic receptor (beta(1)AR) is a major mediator of catecholamine effects in human heart. Catecholamines 67-80 adrenoceptor beta 1 Homo sapiens 4-42 9144094-8 1997 In contrast, catecholamine-induced lipolysis is markedly increased in omental as compared to subcutaneous adipocytes in obese males, mainly due to an increase in beta(3)-adrenoceptor function of visceral fat cells, in combination with a smaller increase in beta(1)-adrenoceptor function. Catecholamines 13-26 adrenoceptor beta 1 Homo sapiens 257-277 11753577-1 2001 BACKGROUND: The beta1-adrenoceptor is a candidate gene for obesity because of its role in catecholamine-induced energy homeostasis. Catecholamines 90-103 adrenoceptor beta 1 Homo sapiens 16-34 11753577-3 2001 OBJECTIVE: To investigate the effect of the Arg 389 Gly beta1-adrenoceptor polymorphism on catecholamine-induced lipolysis in native human fat cells obtained by subcutaneous biopsy. Catecholamines 91-104 adrenoceptor beta 1 Homo sapiens 56-74 10945842-0 2000 Aryloxypropanolamine and catecholamine ligand interactions with the beta(1)-adrenergic receptor: evidence for interaction with distinct conformations of beta(1)-adrenergic receptors. Catecholamines 25-38 adrenoceptor beta 1 Homo sapiens 68-95 10945842-6 2000 Activation of beta(1)-AR by CGP 12177 or LY 362884 was observed to be significantly more resistant to blockade by beta-AR antagonists compared with activation by catecholamines. Catecholamines 162-176 adrenoceptor beta 1 Homo sapiens 14-24 10945842-7 2000 These results suggest that catecholamines and aryloxypropanolamines interact with distinct active conformations of the beta(1)-AR: a state that is responsive to catecholamines and is blocked with high affinity by CGP 12177 and LY 362884, and a novel state that is activated by aryloxypropanolamines but is resistant to blockade by standard beta-AR antagonists. Catecholamines 27-41 adrenoceptor beta 1 Homo sapiens 119-129 10945842-7 2000 These results suggest that catecholamines and aryloxypropanolamines interact with distinct active conformations of the beta(1)-AR: a state that is responsive to catecholamines and is blocked with high affinity by CGP 12177 and LY 362884, and a novel state that is activated by aryloxypropanolamines but is resistant to blockade by standard beta-AR antagonists. Catecholamines 161-175 adrenoceptor beta 1 Homo sapiens 119-129 10212248-1 1999 The beta1-adrenergic receptor (beta1AR) is a key cell surface signaling protein expressed in the heart and other organs that mediates the actions of catecholamines of the sympathetic nervous system. Catecholamines 149-163 adrenoceptor beta 1 Homo sapiens 4-29 10212248-1 1999 The beta1-adrenergic receptor (beta1AR) is a key cell surface signaling protein expressed in the heart and other organs that mediates the actions of catecholamines of the sympathetic nervous system. Catecholamines 149-163 adrenoceptor beta 1 Homo sapiens 31-38 10435003-14 1999 CONCLUSIONS: I(f) expressed in SHR hypertrophied ventricular myocytes is modulated by catecholamines mainly through the stimulation of the beta 1-AR subtype. Catecholamines 86-100 adrenoceptor beta 1 Homo sapiens 139-148 9106627-1 1997 The beta1-adrenergic receptor (beta1-AR) mediates several functions of catecholamines in the heart, including the stimulation of heart rate and contractility. Catecholamines 71-85 adrenoceptor beta 1 Homo sapiens 4-29 9106627-1 1997 The beta1-adrenergic receptor (beta1-AR) mediates several functions of catecholamines in the heart, including the stimulation of heart rate and contractility. Catecholamines 71-85 adrenoceptor beta 1 Homo sapiens 31-39 8697051-1 1995 The control of fat cell lipolysis by the catecholamines involves at least four different adrenoceptor subtypes; three beta (beta 1-, beta 2-, and beta 3-ARs) and one alpha 2-adrenoceptor (alpha 2-AR). Catecholamines 41-55 adrenoceptor beta 1 Homo sapiens 124-156 8697051-8 1995 When considering differential beta-AR recruitment by catecholamines, it is the beta 1-AR which is always activated at the lowest norepinephrine levels, whatever the species, while the activation of the beta 3-AR requires higher norepinephrine levels. Catecholamines 53-67 adrenoceptor beta 1 Homo sapiens 79-88 2547922-1 1989 1) The primary receptor mechanism of catecholamine-induced myocardial potassium uptake is beta 1-adrenoceptor stimulation. Catecholamines 37-50 adrenoceptor beta 1 Homo sapiens 90-109 1600963-2 1992 Patients with chronic congestive heart failure (CHF) show down-regulation of the beta 1-adrenergic receptor with a decrease in receptor density and altered responses to catecholamines. Catecholamines 169-183 adrenoceptor beta 1 Homo sapiens 81-107 1971535-0 1990 Selective beta 1-adrenoceptor blockade enhances positive inotropic responses to endogenous catecholamines mediated through beta 2-adrenoceptors in human atrial myocardium. Catecholamines 91-105 adrenoceptor beta 1 Homo sapiens 10-29 1971535-1 1990 We determined the relative contribution of beta 1- and beta 2-adrenoceptor stimulation to the positive inotropic responses of human atrial myocardium to catecholamines. Catecholamines 153-167 adrenoceptor beta 1 Homo sapiens 43-74 1979934-10 1990 Enoximone thus causes positive inotropic effects and potentiates the effects of catecholamines acting through both beta 1- and beta 2-AR. Catecholamines 80-94 adrenoceptor beta 1 Homo sapiens 115-136 35323624-8 2022 High-level glucose may protect cardiomyocytes from the toxic effects of catecholamine excess through suppressing beta1-adrenoceptor-Gs-PKA signaling. Catecholamines 72-85 adrenoceptor beta 1 Homo sapiens 113-131 2541947-1 1989 The beta 1- and beta 2-adrenergic receptor subtypes are biochemically and functionally similar, because both receptors mediate the catecholamine-dependent activation of adenylate cyclase through the GTP-binding protein, Gs. Catecholamines 131-144 adrenoceptor beta 1 Homo sapiens 4-42 1652275-4 1991 Chronic exposure (days or months), but not acute exposure (hours), to a catecholamine downregulates human heart beta 1AR. Catecholamines 72-85 adrenoceptor beta 1 Homo sapiens 112-120 1652275-7 1991 In human heart, catecholamine-induced activation of one beta 2AR causes the production of at least four times more cyclic AMP than activation of one beta 1AR. Catecholamines 16-29 adrenoceptor beta 1 Homo sapiens 149-157 33093660-4 2021 Structural comparison revealed that the catecholamine-binding pockets are identical between beta1AR and beta2AR, but the extracellular vestibules have different shapes and electrostatic properties. Catecholamines 40-53 adrenoceptor beta 1 Homo sapiens 92-99 2905474-5 1988 Drug treatment aiming to reduce or suppress these processes and their negative results is potentially offered by: vasodilators, counteracting vasoconstriction, low dose selective beta 1-adrenoceptor blockers, which will not only impair tachycardia but also up-regulate cardiac beta 1-receptors and hence improve the inotropic response to catecholamines; aldosterone antagonists and ACE-inhibitors counteracting the activated RAAS. Catecholamines 338-352 adrenoceptor beta 1 Homo sapiens 179-198 2825170-8 1987 Expression of receptor protein in Xenopus laevis oocytes conveys adenylate cyclase responsiveness to catecholamines with a typical beta 1AR specificity. Catecholamines 101-115 adrenoceptor beta 1 Homo sapiens 131-139 391685-2 1979 Their actions are best understood by an appreciation of the relative ability of each catecholamine to activate alpha, beta 1 and beta 2 adrenergic receptors in the myocardium and peripheral vasculature. Catecholamines 85-98 adrenoceptor beta 1 Homo sapiens 111-156 30747396-1 2019 BACKGROUND: Numerous studies have reported significantly elevated titers of serum autoantibody against the second extracellular loop of beta1-adrenoceptor (beta1-AA), a catecholamine-like substance with beta1-adrenergic activity, in patients with heart failure. Catecholamines 169-182 adrenoceptor beta 1 Homo sapiens 136-154 33481407-13 2021 beta1- and beta2-adrenergic receptor antagonists reduced the effects of the catecholamines on transendothelial resistance, whereas alpha-adrenergic receptor antagonists did not. Catecholamines 76-90 adrenoceptor beta 1 Homo sapiens 0-36 32031586-9 2020 CONCLUSION: Given that compartmentalized betaAR signaling can be induced by stress-associated levels of catecholamines, our results revealed an important, yet unappreciated, heart regulation mechanism that is autoadaptive to varied stress conditions. Catecholamines 104-118 adrenoceptor beta 1 Homo sapiens 41-47 31407140-8 2020 When there is a decrease in catecholamine responsiveness, it causes aging in old people because the reduction of betaAR sensitivity and density in the myocardium enhances downregulation of betaARs to AC in the human heart. Catecholamines 28-41 adrenoceptor beta 1 Homo sapiens 113-119 29848777-2 2018 In mammalian cells, catecholamines induce the internalization of the beta1-AR into endosomes and their removal promotes the recycling of the endosomal beta1-AR back to the plasma membrane; however, whether these redistributive processes occur in terminally differentiated cells is unknown. Catecholamines 20-34 adrenoceptor beta 1 Homo sapiens 69-77 24250787-1 2013 beta-blockers are widely used to improve symptoms and prolong life in heart disease primarily by inhibiting the actions of endogenous catecholamines at the beta1-adrenoceptor. Catecholamines 134-148 adrenoceptor beta 1 Homo sapiens 156-174 28522796-2 2017 We wanted to elucidate whether beta1-adrenoceptor-polymorphisms affects the postoperative catecholamine consumption and the length of intermediate care unit stay in patients undergoing cardiac surgery, and whether this might be enhanced or attenuated by catechol-O-methyl-transferase (COMT) polymorphism. Catecholamines 90-103 adrenoceptor beta 1 Homo sapiens 31-49 29063982-1 2018 In the heart, catecholamine effects occur by activation of beta-adrenergic receptors (beta-ARs), mainly the beta 1 (beta1-AR) and beta 2 (beta2-AR) subtypes, both of which couple to the Gs protein that activates the adenylyl cyclase signaling pathway. Catecholamines 14-27 adrenoceptor beta 1 Homo sapiens 116-124 28818208-9 2017 These cellular catecholamine-dependent responses were mainly mediated by beta1-adrenoceptor signaling in TTS. Catecholamines 15-28 adrenoceptor beta 1 Homo sapiens 73-91 26408198-3 2015 By means of a combination of whole-cell patch-clamp and Forster resonance energy transfer (FRET) in single cells, we demonstrate that the activation of the Gs-coupled beta1-adrenoreceptor (beta1-AR) by the catecholamines isoprenaline (Iso) and adrenaline (Adr) is regulated by V(M). Catecholamines 206-220 adrenoceptor beta 1 Homo sapiens 167-187 26408198-3 2015 By means of a combination of whole-cell patch-clamp and Forster resonance energy transfer (FRET) in single cells, we demonstrate that the activation of the Gs-coupled beta1-adrenoreceptor (beta1-AR) by the catecholamines isoprenaline (Iso) and adrenaline (Adr) is regulated by V(M). Catecholamines 206-220 adrenoceptor beta 1 Homo sapiens 189-197 25052258-1 2014 BACKGROUND AND PURPOSE: CGP 12177 not only inhibits agonist effects mediated through the catecholamine site of the beta1 -adrenoceptor with high affinity, but also exhibits agonist effects of its own at higher concentrations through a secondary, low-affinity beta1 -adrenoceptor site or conformation. Catecholamines 89-102 adrenoceptor beta 1 Homo sapiens 115-134 24250787-3 2013 The beta1-adrenoceptor also exists in two agonist conformations - a high affinity catecholamine conformation and a low affinity secondary agonist conformation. Catecholamines 82-95 adrenoceptor beta 1 Homo sapiens 4-22 22975104-15 2012 Elevated response to catecholamines after VAD support is influenced by beta1-AR upregulation and modulation of AC activity. Catecholamines 21-35 adrenoceptor beta 1 Homo sapiens 71-79 22628174-1 2012 Autoantibodies against the second extracellular loop of beta(1) -adrenergic receptor (beta(1) -AA) not only contribute to increased susceptibility to heart failure, but also play a causative role in myocardial remodeling through their catecholamine-like effects via binding with the beta(1) -adrenergic receptor. Catecholamines 235-248 adrenoceptor beta 1 Homo sapiens 56-97 22628174-1 2012 Autoantibodies against the second extracellular loop of beta(1) -adrenergic receptor (beta(1) -AA) not only contribute to increased susceptibility to heart failure, but also play a causative role in myocardial remodeling through their catecholamine-like effects via binding with the beta(1) -adrenergic receptor. Catecholamines 235-248 adrenoceptor beta 1 Homo sapiens 56-84 21159454-2 2011 Excessive amounts of catecholamines released from sympathetic nerve endings as well as from the adrenal medulla under stressful conditions are considered to produce intracellular Ca(2+) overload and cardiac dysfunction through the beta(1)-adrenoceptor signal transduction pathway. Catecholamines 21-35 adrenoceptor beta 1 Homo sapiens 231-251 21311897-1 2011 BACKGROUND: The beta(1)-adrenoceptor (beta(1)AR) mediates cardiostimulatory effects of catecholamines in the heart. Catecholamines 87-101 adrenoceptor beta 1 Homo sapiens 16-36 21311897-1 2011 BACKGROUND: The beta(1)-adrenoceptor (beta(1)AR) mediates cardiostimulatory effects of catecholamines in the heart. Catecholamines 87-101 adrenoceptor beta 1 Homo sapiens 38-47 21311897-2 2011 The Arg389Gly polymorphism of the beta(1)AR gene has recently been shown to determine the responsiveness to catecholamines in vitro, and we previously reported that dobutamine induced an augmented contractile response in humans homozygous for the Arg389 allele. Catecholamines 108-122 adrenoceptor beta 1 Homo sapiens 34-43 19509284-5 2009 Although catecholamine stimulation mediates the retention of beta1AR-EGFR interaction throughout receptor internalization, direct EGF ligand stimulation initiates the internalization of EGFR alone. Catecholamines 9-22 adrenoceptor beta 1 Homo sapiens 61-68 20587416-1 2010 The beta(1)-adrenergic receptor (beta(1)AR) is the predominant betaAR in the heart, mediating the catecholamine-stimulated increase in cardiac rate and force of contraction. Catecholamines 98-111 adrenoceptor beta 1 Homo sapiens 4-42 19509284-7 2009 These data reveal a new signaling paradigm in which beta-arrestin is required for the maintenance of a beta1AR-EGFR interaction that can direct cytosolic targeting of ERK in response to catecholamine stimulation. Catecholamines 186-199 adrenoceptor beta 1 Homo sapiens 103-115 18540901-3 2008 As resorption of foetal lung fluid is a catecholamine dependent process, we aimed at investigating, whether beta1- and beta2-adrenoreceptor (ADRB1, ADRB2) polymorphisms, known to alter catecholamine activity, are operative in TTN. Catecholamines 185-198 adrenoceptor beta 1 Homo sapiens 108-139 19010176-1 2008 INTRODUCTION: Prolonged catecholamine overstimulation of the myocardium in chronic heart failure causes a reduction in the number and functionality of beta1-adrenoceptors (beta1-AR) of the heart. Catecholamines 24-37 adrenoceptor beta 1 Homo sapiens 151-170 19010176-1 2008 INTRODUCTION: Prolonged catecholamine overstimulation of the myocardium in chronic heart failure causes a reduction in the number and functionality of beta1-adrenoceptors (beta1-AR) of the heart. Catecholamines 24-37 adrenoceptor beta 1 Homo sapiens 172-180 19576569-1 2009 In humans, three genes--ADRB1, ADRB2 and ADRB3--encode beta-adrenoreceptors (ADRB); these molecules mediate the action of catecholamines in multiple tissues and play pivotal roles in cardiovascular, respiratory, metabolic, and immunological functions. Catecholamines 122-136 adrenoceptor beta 1 Homo sapiens 24-29 18772317-13 2008 In conclusion, our data with betaAR-G(s)alpha fusion proteins show that endogenous catecholamines and ISO stabilize distinct conformations in the beta(1)AR and beta(2)AR. Catecholamines 83-97 adrenoceptor beta 1 Homo sapiens 146-155 18540901-3 2008 As resorption of foetal lung fluid is a catecholamine dependent process, we aimed at investigating, whether beta1- and beta2-adrenoreceptor (ADRB1, ADRB2) polymorphisms, known to alter catecholamine activity, are operative in TTN. Catecholamines 185-198 adrenoceptor beta 1 Homo sapiens 141-146 17541557-0 2007 In patients chronically treated with metoprolol, the demand of inotropic catecholamine support after coronary artery bypass grafting is determined by the Arg389Gly-beta 1-adrenoceptor polymorphism. Catecholamines 73-86 adrenoceptor beta 1 Homo sapiens 164-183 17541557-3 2007 The aim of this study was to find out whether the Arg389Gly-beta(1)AR polymorphism might also determine demand of catecholamine-induced inotropic support in patients with low cardiac index (CI) after coronary artery bypass grafting (CABG) surgery with cardiopulmonary bypass (CPB). Catecholamines 114-127 adrenoceptor beta 1 Homo sapiens 60-69 17541557-8 2007 We conclude that the Arg389Gly-beta(1)AR polymorphism appears to be a determinant of cardiac responses to catecholamine stimulation. Catecholamines 106-119 adrenoceptor beta 1 Homo sapiens 31-40 18346809-2 2008 The beta1 adrenergic receptor (BAR-1) is a major mediator of catecholamine-induced lipolysis and thermogenesis. Catecholamines 61-74 adrenoceptor beta 1 Homo sapiens 4-29 17211240-12 2007 Plasma CRP concentration in twins was predicted by polymorphisms at three loci in physiological series within the catecholamine biosynthetic/beta-adrenergic pathway: TH (tyrosine hydroxylase), ADRB1 (beta1-adrenergic receptor) and ADRB2 (beta2-adrenergic receptor). Catecholamines 114-127 adrenoceptor beta 1 Homo sapiens 200-225