| URN | urn:agi-Regulation:inout-urn:agi-llid:153:out-urn:agi-meshdis:Heart%20Failure::unknown |
|---|---|
| References | 33 |
| Connectivity | 2 |
| Effect | unknown |
| TextRef | info:pmid/15592928#abs:1 |
|---|---|
| MedLine Reference | 15592928:0 |
| Sentence | The beta-adrenoceptor (beta-AR) plays an important role in heart failure. |
| TextRef | info:pmid/18425130#abs:1 |
|---|---|
| MedLine Reference | 18425130:0 |
| Sentence | Beta-adrenergic receptor (betaAR) blockade is a standard therapy for cardiac failure and ischemia. |
| TextRef | info:pmid/9082678#abs:5 |
|---|---|
| MedLine Reference | 9082678:4 |
| Sentence | Desensitisation of cardiac beta-adrenergic receptors may contribute to contractile dysfunction in chronic heart failure. |
| TextRef | info:pmid/11448139#abs:12 |
|---|---|
| MedLine Reference | 11448139:11 |
| Sentence | These effects may contribute to beta1-adrenoceptor-mediated cardiotoxicity in heart failure. |
| CellType | cardiomyocyte |
| TextRef | info:pmid/14680448#abs:1 |
|---|---|
| MedLine Reference | 14680448:0 |
| Sentence | Carvedilol and metoprolol are beta(1)-adrenoceptor antagonists that decrease mortality in heart failure. |
| TextRef | info:pmid/12357106#abs:2 |
|---|---|
| MedLine Reference | 12357106:1 |
| Sentence | The catecholamines, via alpha- and beta-adrenergic receptor (beta-AR) stimulation, may play a role in the development of heart failure. |
| TextRef | info:pmid/12197595#abs:1 |
|---|---|
| MedLine Reference | 12197595:0 |
| Sentence | Beta-1-adrenergic receptor (beta1-AR) blockers reduce both the incidence of sudden death and the ventricular volume in heart failure. |
| TextRef | info:pmid/11807612#abs:2 |
|---|---|
| MedLine Reference | 11807612:1 |
| Sentence | In vitro studies have shown down-regulation of beta-AR density in heart failure and cardiac conditions that may lead to heart failure. |
| TextRef | info:pmid/9456285#abs:8 |
|---|---|
| Organ | ventricle |
| MedLine Reference | 9456285:7 |
| Sentence | In the right ventricle, beta1-adrenoceptor density decreased only in heart failure; beta2-adrenoceptor density was unchanged. |
| TextRef | info:pmid/19103994#abs:1 |
|---|---|
| MedLine Reference | 19103994:0 |
| Sentence | Chronic stimulation of the beta(1)-adrenoceptor (beta(1)AR) plays a crucial role in the pathogenesis of heart failure; however, underlying mechanisms remain to be elucidated. |
| TextRef | info:pmid/12954981#abs:2 |
|---|---|
| MedLine Reference | 12954981:1 |
| Sentence | In addition to regulating cardiac rate and contractility, beta1AR and beta2AR may play different roles in the pathogenesis of heart failure. |
| TextRef | info:pmid/18947427#abs:1 |
|---|---|
| Organ | Heart |
| MedLine Reference | 18947427:0 |
| Sentence | Persistent stimulation of cardiac beta1-adrenergic receptors by endogenous norepinephrine promotes heart failure progression. |
| TextRef | info:pmid/12422153#abs:1 |
|---|---|
| Organ | Heart |
| MedLine Reference | 12422153:0 |
| Sentence | Exercise performance in patients with congestive heart failure is partially dependent on cardiac beta1-adrenergic receptor (beta1AR) function. |
| TextRef | info:pmid/10086986#abs:10 |
|---|---|
| Organ | Heart |
| MedLine Reference | 10086986:9 |
| Sentence | In summary, xamoterol and bucindolol, but not carvedilol and bisoprolol, exhibited direct beta1-adrenoceptor-mediated ISA in normal and heart failure rats. |
| TextRef | info:pmid/11964375#abs:1 |
|---|---|
| MedLine Reference | 11964375:0 |
| Sentence | Chronic stimulation of the beta(1)-adrenergic receptor leads to hypertrophy and heart failure in beta(1)-adrenergic receptor transgenic mice and contributes to disease progression in heart failure patients. |
| TextRef | info:pmid/18615004#abs:1 |
|---|---|
| MedLine Reference | 18615004:0 |
| Sentence | Numerous studies have demonstrated that beta(1)- and beta(2)-adrenergic receptor gene (ADRB1 and ADRB2) variants influence cardiovascular risk and beta-blocker responses in hypertension and heart failure. |
| TextRef | info:pmid/12689818#abs:2 |
|---|---|
| Organ | Heart |
| MedLine Reference | 12689818:1 |
| Sentence | We have, recently, shown that heart-specific overexpression of the beta(1)-adrenergic receptor in transgenic mice (TG) initially leads to increased contractility, followed by LV hypertrophy and heart failure. |
| TextRef | info:pmid/17278500#abs:1 |
|---|---|
| Organ | Heart |
| MedLine Reference | 17278500:0 |
| Sentence | Myocardial beta adrenergic receptor (beta-AR) concentration can substantially decrease in congestive heart failure and significantly increase in chronic volume overload, such as in severe aortic valve regurgitation. |
| TextRef | info:pmid/16807128#abs:2 |
|---|---|
| Organ | Heart |
| MedLine Reference | 16807128:1 |
| Sentence | Normalization of betaAR signalling consistently ameliorates cardiac dysfunction and survival in heart failure, suggesting that betaAR dysfunction may be intrinsically linked to the deterioration of cardiac performance. |
| TextRef | info:pmid/17336757#abs:1 |
|---|---|
| Organ | Heart |
| MedLine Reference | 17336757:0 |
| Sentence | The beta2/beta1 adrenoceptor ratio increases in congestive heart failure (CHF), making the heart relatively more dependent on inotropic, lusitropic, and chronotropic stimulation by the beta2-adrenergic receptor (ADRB2). |
| TextRef | info:pmid/18585502#abs:4 |
|---|---|
| Organ | Heart |
| MedLine Reference | 18585502:3 |
| Sentence | We analyzed the distribution of autoantibodies against Kv channel-interacting protein (KChIP) 2.6, cardiac troponin I (cTnI), and the beta1-adrenergic receptor (second extracellular loop, cardiac beta1-adrenergic receptor [SEL-beta1-AR])-two other known autoantibodies involved in heart failure. |
| TextRef | info:pmid/15979723#abs:7 |
|---|---|
| Organ | Heart |
| MedLine Reference | 15979723:6 |
| Sentence | In this review, we attempt to highlight the distinct functionalities and signaling mechanisms of these betaAR subtypes and discuss how these subtype-specific properties of betaARs might affect the pathogenesis of congestive heart failure (CHF) and the therapeutic effectiveness of certain beta-blockers in the treatment of congestive heart failure. |
| TextRef | info:pmid/1323000#abs:2 |
|---|---|
| Organ | Heart |
| MedLine Reference | 1323000:1 |
| Sentence | With the use of delta Vcfc, a load independent parameter of myocardial contraction, AR mediated contraction was evaluated. beta-AR mediated contraction, delta Vcfc by infusion of a beta-AR agonist, isoproterenol, declined with the advancement of heart failure from 0.41 Circ/sec (NYHA I) to 0.31 (NYHA II), 0.22 (NYHA III) and 0.12 (NYHA IV). |
| TextRef | info:pmid/17158652#cont:201 |
|---|---|
| Organ | Heart |
| MedLine Reference | 17158652:10200 |
| Sentence | Both apoptosis and ß-AR downregulation are both thought to play a key role in the progression of heart failure. |
| Journal | Heart Circul |
| Journal Reference | v292 i4 p1898 |
| Journal Link | http://ajpheart.physiology.org/cgi/content/full/292/4/H1898 |
| TextRef | info:pmid/17369456#cont:236 |
|---|---|
| Organ | Heart |
| MedLine Reference | 17369456:10235 |
| Sentence | Animals with disruption of PI3K? gene are protected from chronic ß-AR stimulation-induced heart failure ( 33 ). |
| Journal | Heart Circul |
| Journal Reference | v293 i1 p385 |
| Journal Link | http://ajpheart.physiology.org/cgi/content/full/293/1/H385 |
| TextRef | info:pmid/17925438#cont:24 |
|---|---|
| MedLine Reference | 17925438:10023 |
| Sentence | The ßAR antagonist carvedilol recently was demonstrated to significantly reduce morbidity and mortality in heart failure and in post-AMI patients ( 22 – 25 ). |
| CellLineName | AMI |
| Journal | PNAS |
| Journal Reference | v104 i42 p16657 |
| Journal Link | http://www.pnas.org/content/104/42/16657.full |
| TextRef | info:pmid/16699071#cont:22 |
|---|---|
| Organ | Nervous system |
| MedLine Reference | 16699071:10021 |
| Sentence | Moreover, ß-adrenergic receptor (ß-AR) antagonists have been shown to reduce post-MI remodeling and heart failure development and to improve patients' outcome ( 2 , 19 ). |
| Journal | Heart Circul |
| Journal Reference | v291 i4 p1754 |
| Journal Link | http://ajpheart.physiology.org/cgi/content/full/291/4/H1754 |
| TextRef | info:pmid/12711600#cont:271 |
|---|---|
| Organ | Heart |
| MedLine Reference | 12711600:10270 |
| Sentence | These results appear to conflict with observations that betaAR antagonists can reduce fibrosis in heart failure ( 37 , 38 ). |
| CellType | fibroblast |
| Journal | J. Biol. Chem |
| Journal Reference | v278 i27 p24461 |
| Journal Link | http://www.jbc.org/cgi/content/full/278/27/24461 |
| TextRef | info:pmid/16186489#cont:15 |
|---|---|
| Organ | Heart |
| MedLine Reference | 16186489:10014 |
| Sentence | Many clinical trials have indicated that angiotensin-converting enzyme inhibitors and ß-AR blockers significantly improve the survival rates of heart failure patients by decreasing cardiac remodeling ( 8 ). |
| Journal | PNAS |
| Journal Reference | v102 i41 p14771 |
| Journal Link | http://www.pnas.org/cgi/content/full/102/41/14771 |
| TextRef | info:pmid/15569686#cont:262 |
|---|---|
| Organ | Heart |
| MedLine Reference | 15569686:10261 |
| Sentence | In line with this hypothesis, long term treatment with ß-AR antagonists improves prognosis and cardiac function in heart failure patients ( 47 ), whereas ß-AR agonists increase mortality in these patients ( 48 ). |
| Tissue | Plasma |
| Journal | J. Biol. Chem |
| Journal Reference | v280 i8 p6906 |
| Journal Link | http://www.jbc.org/cgi/content/full/280/8/6906 |
| TextRef | info:pmid/15001662#cont:225 |
|---|---|
| MedLine Reference | 15001662:10224 |
| Sentence | The latter authors hypothesized that a 2C - and ß 1 -AR polymorphisms act synergistically to increase synaptic NE release and yield enhanced receptor function, respectively, so as to decrease cardiac function and promote progression of heart failure. |
| CellLineName | GLY |
| Journal | Pharm. Rev |
| Journal Reference | v56 i1 p31 |
| Journal Link | http://pharmrev.aspetjournals.org/cgi/content/full/56/1/31 |
| TextRef | info:pmid/16204467#cont:131 |
|---|---|
| Organ | Heart |
| MedLine Reference | 16204467:10130 |
| Sentence | Thus, transgenic overexpression of ß 1 -adrenergic receptors in mice leads to cardiac hypertrophy, heart failure, and early death, whereas, overexpression of the ß 2 -adrenergic receptor actually improves cardiac function and does not adversely affect life span (Xiao et al., 1999b ). |
| Journal | Mol. Pharm |
| Journal Reference | v69 i1 p5 |
| Journal Link | http://molpharm.aspetjournals.org/cgi/content/full/69/1/5 |
| TextRef | info:pmid/15319203#cont:131 |
|---|---|
| Organ | Heart |
| MedLine Reference | 15319203:10130 |
| Sentence | The model of increased cavity volumes studied by us is particularly relevant, as it is well recognized that chronic ß-AR activation occurs in chronic heart failure and contributes to increases in cavity volumes and that ß-AR blocking agents reduce cardiac cavity volumes in chronic heart failure ( 5 , 16 ). |
| Journal | Heart Circul |
| Journal Reference | v287 i6 p2762 |
| Journal Link | http://ajpheart.physiology.org/cgi/content/full/287/6/H2762 |