TY - JOUR. T1 - Skin fibroblast beta-adrenergic receptor function in manie-depressive illness. AU - Berrettini, Wade H.. AU - Bardakjian, Josiane. AU - Cappellari, Charles B.. AU - Barnett, Arthur L.. AU - Albright, Allen. AU - Nurnberger, John I.. AU - Gershon, Elliot S.. PY - 1987/12. Y1 - 1987/12. N2 - Beta-adrenergic receptor function was assessed in cultured skin fibroblasts obtained from bipolar patients and normal volunteers by measurement of the cyclic adenosine monophosphate (cAMP) response to isoproterenol. No group differences were observed. To assess regulation of receptor desensitization, fibroblasts were incubated for 24 hr with isoproterenol, and then the cAMP response to isoproterenol was determined. Subsensitivity to rechallenge with isoproterenol did not distinguish bipolar patients from controls.. AB - Beta-adrenergic receptor function was assessed in cultured skin fibroblasts obtained from bipolar patients and normal volunteers by measurement of the cyclic adenosine ...
TY - JOUR. T1 - Impaired beta-adrenergic receptor activation of adenylyl cyclase in airway smooth muscle in the basenji-greyhound dog model of airway hyperresponsiveness.. AU - Emala, C.. AU - Black, C.. AU - Curry, C.. AU - Levine, M. A.. AU - Hirshman, C. A.. PY - 1993/6. Y1 - 1993/6. N2 - Previous studies in human asthmatics have suggested a defect in the beta-adrenergic pathway leading to cyclic adenosine monophosphate (cAMP) generation. Although these studies have suggested normal or increased numbers of beta-adrenergic receptors, limitations in the quantity of tissue available have not allowed further delineation of the biochemical or molecular mechanisms of human asthma. The basenji-greyhound (BG) dog model of nonspecific airway hyperreactivity displays similarities to human asthma, and altered functional response to beta-adrenergic agonists has been previously shown in airway tissue from this model. We have now correlated this functional impairment in beta-adrenergic response with a ...
The present study was carried out to determine, first, the cardiac beta -adrenergic receptor characteristics of normal chickens and chickens with heart failure and, second, the characteristics of myocardial beta -adrenergic receptors in non-hypertrophied hearts in broilers exposed to two different altitude and temperature programmes. The density of beta -adrenergic receptors was significantly lower in myocardial cells in right ventricular failure birds compared with healthy birds. The binding capacity of beta -adrenergic receptors was reduced in the non-hypertrophied ventricles after exposure to high altitude in the younger but not in older chickens. At both altitudes, beta -adrenergic receptor binding capacity was not significantly different in low temperature compared with normal temperature birds. These data support the hypothesis of beta -adrenergic receptor downregulation as one of the mechanisms of cardiac cell adaptation to hypertrophy or hypoxia. Second, the acclimatization to high ...
METHODS AND RESULTS We examined the beta-adrenergic receptor-responsive adenylyl cyclase pathway in hearts from pigs subjected to volume-overload hypertrophy with circulatory congestion. Nine pigs underwent initial pharmacological and hemodynamic studies, and, 5 weeks after aortocaval fistula placement, when signs of circulatory congestion were evident, these measurements were repeated. Biochemical analyses of plasma and myocardium from these animals and seven normal animals were compared. Experimental animals showed signs of circulatory congestion (tachypnea, weight gain, pulmonary rales) within 3-4 weeks of fistula placement. Necropsy showed ascites and biventricular cardiac hypertrophy, but no fibrosis or inflammation was present on histological inspection. Heart rate responsiveness to beta AR stimulation was blunted, with ED50, for isoproterenol increased 133% (p less than 0.001) after development of circulatory congestion. Biochemical analyses of the beta AR-responsive adenylyl cyclase ...
Adrenergic beta-blocking agents were given to 7 patients with advanced congestive cardiomyopathy who had tachycardia at rest (98 plus or minus 13 beats/min). The patients were on beta-adrenergic receptor blockade for 2 to 12 months (average 5-4 months). One patient was given alprenolol 50 mg twice daily and the other patients were given practolol 50 to 400 mg twice daily. Virus infection had occurred in 6 of the patients before the onset of symptoms of cardiac disease. All patients were in a steady state or were progressively deteriorating at the start of beta-adrenergic receptor blockade. Conventional treatment with digitalis and diuretics was unaltered or reduced during treatment with beta-blocking agents. An improvement was seen in their clinical condition shortly after administration of the drugs. Continued treatment resulted in an increase in physical working capacity and a reduction of heart size. Noninvasive investigations including phonocardiogram, carotid pulse curve, apex cardiogram, ...
Metoprolol is classified as a type of beta blocker. This drug reduces how hard the heart needs to work to get blood pumped throughout the body. This helps to decrease blood pressure and the demand for oxygen. When you important site take this medication, some of the messages going to your heart from the nerves are stopped. This is because the beta-adrenergic receptors are blocked, not allowing these messages to be received by your heart. This reduces the force and workload of your heart by reducing your heart rate ...
Combining with epinephrine or norepinephrine to initiate a change in cell activity via activation of a G protein, with pharmacological characteristics of beta-adrenergic receptors; the activity involves transmitting the signal to the Gs alpha subunit of a…
The focus of work in this laboratory is on the elucidation of the molecular properties and regulatory mechanisms controlling the function of G protein-coupled receptors. As model systems we utilize the so called adrenergic receptors for adrenaline and related molecules. The goal is to learn the general principles of signal transduction from the outside to the inside of the cell which are involved in systems as diverse as sensory perception, neuro- transmitter and hormonal signaling. Studies are performed with isolated protein, whole cells in culture and even in vivo in whole animals.
The focus of work in this laboratory is on the elucidation of the molecular properties and regulatory mechanisms controlling the function of G protein-coupled receptors. As model systems we utilize the so called adrenergic receptors for adrenaline and related molecules. The goal is to learn the general principles of signal transduction from the outside to the inside of the cell which are involved in systems as diverse as sensory perception, neuro- transmitter and hormonal signaling. Studies are performed with isolated protein, whole cells in culture and even in vivo in whole animals.
The interaction of the renin-angiotensin system and the sympathetic nervous system in patients with congestive heart failure is not well understood. We tested the hypothesis that angiotensin-converting enzyme inhibitors can resensitize the beta-adrenergic receptor system. Guinea pigs were given captopril, isoproterenol, or both for 2 weeks. At death, cardiac sarcolemmal and light vesicle fractions and intact mononuclear leukocytes were prepared. Captopril treatment led to an up-regulation of cardiac beta 1- but not mononuclear leukocyte beta 2-adrenergic receptors and an increase in isoproterenol-stimulated adenylate cyclase activity in the heart. Animals treated with isoproterenol developed cardiac hypertrophy, had increased plasma norepinephrine levels, and had a decreased number and responsiveness of both cardiac and mononuclear leukocyte beta-adrenergic receptors. Concomitant treatment with captopril attenuated alterations of heart weight, plasma norepinephrine levels, and cardiac ...
We have recently described the affinity chromatography purification of the turkey erythrocyte beta-adrenergic receptor. The minute amounts obtained initially precluded extensive biochemical characterization. To improve the yield of the receptor, the erythrocyte membranes have been prepared by a new method. This procedure resulted in a 10-fold higher receptor density in comparison with the membrane preparation used previously. The new membranes also contained a catecholamine-sensitive guanine triphosphatase and an adenylate cyclase sensitive to Gpp(NH)p and l-epinephrine. Solubilization by a double digitonin extraction resulted in a preparation containing 4-6 pmoles of 3H-dihydroalprenolol binding sites per mg of membrane protein. A single step of affinity chromatography on alprenolol-sepharose of the soluble digitonin extract resulted in an additional 1,000-fold purification of the receptor. The overall purification factor was 20,000 relative to the binding activity of the crude membrane ...
Repeated administration of the centrally acting beta adrenoceptor agonist, clenbuterol, to rats reduced the ability of isoproterenol to increase the concentration of cyclic AMP (cAMP) in slices of cerebellum. This reduced responsiveness to isoproterenol was accompanied by a marked reduction in the density of beta adrenoceptors as measured by the binding of the beta adrenoceptor antagonist [125I]iodopindolol. In addition, the agonist-binding properties of remaining cerebellar beta adrenoceptors were altered after clenbuterol treatment. The clenbuterol-induced reduction in the density of beta adrenoceptors in the cerebellum is in marked contrast to its inability to do this in cerebral cortex. Comparison of the ability of clenbuterol to that of isoproterenol to increase levels of cAMP in slices of cerebral cortex or cerebellum showed that clenbuterol is a weakly potent agonist in both brain regions. The increase in cAMP induced by isoproterenol in the cortex was significantly reduced in the ...
Additional patient-specific factors to consider in the development of an individualized treatment plan include the disease stage, disease-related complications, life expectancy, and the risk of adverse drug effects. Major concerns with BG management in older adults are hypoglycemia-which is the most important factor in determining glycemic goals-and hyperglycemia.1. Hypoglycemia and Hyperglycemia: Too often, tight BG control is inappropriately applied to a frail, vulnerable LTC population, resulting in profound hypoglycemia and ADL impairment, falls, arrhythmias, and death.10-13 Risk factors for developing hypoglycemia include neurologic disease (i.e., stroke, transient ischemic attack, dementia, cognitive impairment), heart failure, depression, sulfonylurea use, insulin, advanced age, impaired renal function, slowed hormonal regulation and counterregulation, decreased hepatic-enzyme activity, reduced beta-adrenergic receptor function, decreased or inconsistent nutritional intake, polypharmacy, ...
G-protein-linked receptor. Illustration of G-protein-mediated intracellular signalling. A chemical signal (ligand, orange, upper left) attaches to a receptor (red) in the cell membrane (blue). This causes the receptor to bind to a G-protein (yellow). A series of reactions is triggered and the G-protein activates a membrane enzyme called adelynate cyclase (red, centre right). Further reactions involving cAMP (cyclic adenosine monophosphate), various enzymes, and ATP (adenosine triphosphate), result in the target protein (bottom right, yellow) being phosphorylated, controlling its activity. For this artwork with labels, see C023/8845. - Stock Image C023/8846
Propranolol, the first beta-adrenergic receptor blocking agent to receive approval from the Food and Drug Administration for marketing, will soon be available for general use in the United States. Because of the mass of information that has accumulated relating to the physiological, metabolic, and clinical effects of this type of pharmacologic agent (1), great interest has developed in the clinical application of beta-adrenergic receptor inhibition. However, the widespread enthusiasm attendant upon the imminent availability of drugs that can specifically block beta receptors should be tempered. Although these agents have been shown to have considerable therapeutic efficacy, there is ample evidence ...
BioAssay record AID 47971 submitted by ChEMBL: In vivo beta adrenergic receptor blocking potency was determined by inhibition of tachycardia produced by isoproterenol (0.2 mg/kg iv) in cat preparation.
Human serotonin [5-hydroxytryptamine (5-HT)1A] receptors have been transfected in NIH-3T3 cells, and their pharmacology and coupling to adenylyl cyclase have been analyzed. Three cellular preparations were used, 1) monoclonal cell lines (clones 6, 2B, and 4B), expressing 45, 280, and 500 fmol of 5-HT1A receptors/mg of protein, respectively; 2) clones 6, 2B, and 4B in which the concentration of 5-HT1A receptors was increased after stimulation of the glucocorticoid-inducible promoter with dexamethasone; and 3) polyclonal cell lines that expressed an increasing amount of 5-HT1A receptor as a function of cell passage. The transfected 5-HT1A receptors inhibited basal, forskolin-stimulated, and isoproterenol-stimulated adenylyl cyclase. The inhibition was dependent on the receptor density expressed, increasing from 60% at low density (45 fmol/mg) to 90% at a density higher than 280 fmol/mg. The pharmacology of the 5-HT1A receptor was studied, with particular attention being paid to the behavior of ...
Desipramine-yohimbine combination treatment of refractory depression. Implications for the beta-adrenergic receptor hypothesis of antidepressant action ...
Semantic Scholar extracted view of Role of beta-adrenergic receptors in counterregulation to insulin-induced hypoglycemia. by Ethan Abramson et al.
p>The checksum is a form of redundancy check that is calculated from the sequence. It is useful for tracking sequence updates.,/p> ,p>It should be noted that while, in theory, two different sequences could have the same checksum value, the likelihood that this would happen is extremely low.,/p> ,p>However UniProtKB may contain entries with identical sequences in case of multiple genes (paralogs).,/p> ,p>The checksum is computed as the sequence 64-bit Cyclic Redundancy Check value (CRC64) using the generator polynomial: x,sup>64,/sup> + x,sup>4,/sup> + x,sup>3,/sup> + x + 1. The algorithm is described in the ISO 3309 standard. ,/p> ,p class="publication">Press W.H., Flannery B.P., Teukolsky S.A. and Vetterling W.T.,br /> ,strong>Cyclic redundancy and other checksums,/strong>,br /> ,a href="http://www.nrbook.com/b/bookcpdf.php">Numerical recipes in C 2nd ed., pp896-902, Cambridge University Press (1993),/a>),/p> Checksum:i ...
The beta-adrenergic receptor kinase (beta ARK) phosphorylates the agonist-occupied beta-adrenergic receptor to promote rapid receptor uncoupling from Gs, thereby attenuating adenylyl cyclase activity. Beta ARK-mediated receptor ...
Mostly used as a bronchodilator that widens the air passages in your lungs, terbutaline has many other uses because of the fact that it attaches to the beta-adrenergic receptors on any muscle cells and makes them relax. First approved by the FDA in 1974, more.... Brand name(s): Brethine ...
Wet-lab validated real-time PCR primer assays for your biological pathway of interest. Select your gene target of interest using an interactive pathway map, and select your plate.
Wet-lab validated real-time PCR primer assays for your biological pathway of interest. Select your gene target of interest using an interactive pathway map, and select your plate.
My hourly rate is $75 an hour. I do have a sliding scale fee system. I take cash, check and credit cards.. Jane Lefkowitz, LICSW. ...
Beta blockers are used to treat certain types of heart-related problems. Learn about the benefits of using beta blockers from Discovery Health.
ISO 62:1999, ISO 75-2:1993, ISO 178:1993, ISO 179:1993, ISO 180:1993, ISO 293:1986, ISO 294-1:1996, ISO 306:1994, ISO 527-2:1993, ISO 527-4:1997, ISO 899-1:1993, ISO 1133:1997, ISO 1183:1987, ISO 1656:1996, ISO 2561:1974, ISO 2580-1, ISO 2818:1994, ISO 3167:1993, ISO 4581:1994, ISO 4589:1984, ISO 8256:1990, ISO 10350:1993, ISO 11357-2:1999, IEC 60093:1980, IEC 60112:1979, IEC 60243-1:1998, IEC 60250:1969, IEC 60296:1982, IEC 60695-11-10:1999, EN ISO 62:1999, EN ISO 75-2:1996, EN ISO 293:2003, EN ISO 294-1:1998, EN ISO 306:1996, EN ISO 527-2:1996, EN ISO 527-4:1997, EN ISO 1133:1999, EN ISO 2818:1996, EN ISO 8256:1996 ...
Purified sarcolemmal and light vesicle (intracellular) fractions of beta-adrenergic receptors were used to examine the effects of propranolol on receptor translocation in guinea pig heart. Guinea pigs were given propranolol (0.15 mg/kg/hr) via minipumps for 7 days and either killed or made ischemic for 1 hour via a coronary ligature. Propranolol treatment led to an externalization of beta-receptors from light vesicle to sarcolemmal fractions. This externalization increased the number of surface beta-adrenergic receptors that were functional, as assessed by isoproterenol-stimulated adenylate cyclase activity. After chronic propranolol treatment, ischemia did not further alter receptor distribution. These results suggest that externalization of beta-adrenergic receptors from a light vesicle fraction to the sarcolemma contributes to up-regulation of beta-receptors that occur in response to both propranolol treatment and ischemia. Because propranolol-treated animals show blunting in externalization ...
Treatment of rats with chemical carcinogens, including 2-acetylaminofluorene (2-AAF), leads to a strong increase in the hepatic catecholamine-sensitive adenylate cyclase activity. The present study was undertaken to investigate the mechanism for the development of this increase. We report that hepatocytes isolated from rats which had been fed 2-AAF (0.025% w/w) for 8-12 weeks had an increased number of β-adrenoceptors, as determined by [3H]dihydroalprenolol binding to whole cells and [125I]iodocyanopindolol binding to washed particles. For both ligands the number of binding sites was about 4-fold higher in hepatocytes from 2-AAF-treated rats than in those from controls. The adenylate cyclase activity of the carcinogen-fed animals showed both a general increase manifested in the basal level (2-fold) and in the activities obtained by stimulation with guanine nucleotides (2-3-fold), cholera toxin (1.5-fold), and glucagon (1.3-fold) and a selective, larger increase in the β-adrenoceptor-linked ...
Exercise training and beta-blocker treatment ameliorate age-dependent impairment of beta-adrenergic receptor signaling and enhance cardiac responsiveness to adrenergic stimulation. Am J Physiol Heart Circ Physiol 293: H1596-H1603, 2007. First published June 8, 2007; doi:10.1152/ajpheart.00308.2007.- Cardiac beta-adrenergic receptor (*-AR) signaling and left ventricular (LV) responses to beta-AR stimulation are impaired with aging. It is shown that exercise and beta-AR blockade have a favorable effect on cardiac and vascular *-AR signaling in several cardiovascular diseases. In the present study, we examined the effects of these two different strategies on *-AR dysregulation and LV inotropic reserve in the aging heart. Forty male Wistar-Kyoto aged rats were randomized to sedentary, exercise (12 wk treadmill training), metoprolol (250 mg kg-1 day-1 for 4 wk), and exercise plus metoprolol treatment protocols. Ten male Wistar- Kyoto sedentary young rats were also used as a control group. Old ...
Minaprine is an amino-phenylpyridazine antidepressant reported to be relatively free of cardiotoxicity, drowsiness, and weight gain. Similar to other antidepressant treatments, minaprine attenuates the beta-adrenergic receptor function. Studies have also shown that minaprine improves memory consolidation and that repeated drug administration leads to potentiation of this effect. Moreover, the effects of minaprine on memory consolidation are related to its dopaminergic action ...
Beta adrenergic receptor kinase carboxyl-terminus (also βARKct) is a peptide composed of the last 194 amino acid residues of the carboxyl-terminus of beta adrenergic receptor kinase 1 (βARK1). It binds the βγ subunits of G proteins located in the plasma membrane of cells. It is currently an experimental gene therapy for the treatment of heart failure. During heart failure, the heart is not able to pump enough blood to the rest of the body and will begin to undergo processes in order to compensate for its decreased function. These processes will attempt to increase the hearts output; however, the heart may become overstressed and eventually dysfunctional as a result. The sympathetic nervous system increases norepinephrine release to stimulate β-adrenergic receptors (βARs) located on heart cell (cardiomyocyte) membranes to increase the hearts rate and force of contraction. If the heart is already stressed or damaged, this will cause the heart to work above its capacity. Continuous ...
Macrophages play an integral role in eliminating infection during the inflammatory response. Catecholamines are known to alter macrophage function by binding to adrenergic receptors on the macrophage membrane. Stimulation through β-adrenergic receptors (β-AR) is known to decrease macrophage function while stimulation through the α-adrenergic receptor (α-AR) is thought to have a stimulatory effect on immune function. The RAW264.7 murine macrophage cell line is used as a model of macrophage function, but little is known about the expression of adrenergic receptors on these cells. In these studies, macrophages were treated with the catecholamine norepinephrine, the non-selective α-adrenergic receptor agonist clonidine, or the selective α2-adrenergic receptor antagonist RS79948 (RS), prior to lipopolysaccharide (LPS) activation, and then analyzed for the production of the proinflammatory cytokines TNF-α and IL-6. Low concentrations of clonidine increased cytokine production while RS reversed these
TY - JOUR. T1 - Potentiated anaphylaxis in patients with drug-induced beta-adrenergic blockade. AU - Jacobs, Robert L.. AU - Rake, Geoffrey W.. AU - Fournier, Donald C.. AU - Chilton, Robert J. AU - Culver, William G.. AU - Beckmann, Charles H.. PY - 1981. Y1 - 1981. N2 - Anaphylaxis to known allergens occurred in two patients under treatment for hypertension with propranolol. The clinical course of both cases was similar. Bradycardia associated with an undetectable blood pressure, unusual severity, and sluggish response to treatment were major common factors in which blockade of the beta-adrenergic system may have had a role. Propranolol, a beta-adrenergic antagonist that acts competitively by blocking the adenylate cyclase receptor on efferent cells, is well recognized to cause increased airways resistance in some asthmatic and normal subjects. It is postulated that propranolol potentiated anaphylaxis in these patients by inhibition of adenylate cyclase, resulting in lowered intracellular ...
To more fully characterize the alterations in myocardial adrenergic and cholinergic receptors induced by the diabetic state, we investigated the binding characteristics of (-) [3H] dihydroalprenolol to beta adrenergic receptors (bAR), [3H] prazosin to alpha adrenergic receptors (aAR), and [3H] quinuclidinyl-benzilate to muscarinic cholinergic receptors (MCR) in myocardial membranes derived from rats 8 wk after treatment with streptozotocin. We also studied an equal number of animals from three control groups: free-eating nondi-abetics, pair-weighted nondiabetics, and streptozoto-cin-treated animals treated daily with insulin.. Diabetic hearts demonstrated 27% fewer bAR (P , 0.01) and 31% fewer aAR (P , 0.01) than free-eating controls, without changes in MCR, and without changes in antagonist affinity, agonist affinity, or agonist slope factor (pseudo-Hill coefficient) for any class of receptors. Food restriction had no effect on receptor characteristics, and treatment of diabetic rats with ...
Brodde OE, Karad K, Zerkowski HR, Rohm N, Reidemeister JC (1983). „Coexistence of beta 1- and beta 2-adrenoceptors in human right atrium. Direct identification by (+/-)-[125I]iodocyanopindolol binding". Circulation Research. 53 (6): 752-758. PMID 6139182 ...
Sobolev A., Rosenkranz A., Kazarov A. A study of mechanisms of post-irradiation changes in adenylate-cyclase activity // International journal of radiation biology and related studies in physics, chemistry, and medicine. - 1983. - Vol. 44, no. 1. - P. 31-39. Hormone-stimulated adenylate-cyclase activity (via beta-adrenergic receptors) is reduced after in vitro irradiation of plasma membranes of frog erythrocytes, at a dose (650 Gy) which does not change the number of beta-adrenergic receptors but causes an oxidative degradation of membrane lipids. Peroxidation of membrane lipids without irradiation also results in a lesser stimulation of adenylate cyclase by the beta-agonist. A possible mechanism of change in adenylate-cyclase functioning is discussed. [ DOI ...
riverbabble, a short story and poetry literary journal and e-zine (published June and January), features the work of writer.
The Department of Psychiatry at the University of Pennsylvania is committed to the tripartite mission of providing the highest level of care to patients, conducting innovative research, and educating the future leaders in the field.
Stimulation of Gi-coupled receptors leads to the activation of mitogen-activated protein kinases (MAP kinases). In several cell types, this appears to be dependent on the activation of p21ras (Ras). Which G-protein subunit(s ...
p66 beta 兔多克隆抗体(ab76925)可与小鼠, 人样本反应并经WB, IP, IHC实验严格验证。中国75%以上现货,所有产品均提供质保服务,可通过电话、电邮或微信获得本地专属技术支持。
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EN482, EN45544-2:1999, EN45544-3:1999, EN50270, EN60073, EN60068-2-6, ISO 3534-1, ISO 6141, ISO 6142, ISO 6143, ISO 6144, ISO 6145-1, ISO 6145-3, ISO 6145-4, ISO 6145-6, ISO 6147, ISO 6879:1995, ISO 7504 ...
beta 1- and beta 2-Adrenergic receptors co-exist in the adult rat ventricle. We have employed radioligand binding and cell purification techniques to determine the cellular origin of these receptors. The beta-adrenergic antagonist ligand (+/-)-[125I] iodocyanopindolol binds to 2 X 10(5) receptors per purified adult rat cardiomyocyte, with a dissociation constant of 70 pM. The subtype-selective antagonists betaxolol (beta 1), practolol (beta 1), and zinterol (beta 2) compete for [125I]iodocyanopindolol-binding sites on intact myocytes in monophasic manners with dissociation constants of 46, 845, and 923 nM, respectively. [125I]iodocyanopindolol binding to membranes prepared from nonmyocyte elements of rat ventricle occurs with a dissociation constant of 43 pM and a capacity of 88 fmol/mg membrane protein. Computer analysis of competition of [125I]iodocyanopindolol binding by betaxolol, practolol, and zinterol in nonmyocyte membranes demonstrates biphasic curves that comprise binding to both beta ...
The deubiquitinase ubiquitin-specific protease 20 is a positive modulator of myocardial β1-adrenergic receptor expression and signaling.
Rapid eye movement (REM) sleep deprivation induces a cortical down-regulation of beta-adrenergic receptors. Down-regulation of cortical beta-adrenergic receptors is consistently observed after a number of different chronic antidepressant treatments (drugs and electroconvulsive shock). REM sleep deprivation has an antidepressant effect in humans, and in rats, it decreases immobility in the behavioral despair test, an effect also produced by antidepressant treatments. To verify whether REM sleep deprivation also affects hippocampal beta-adrenergic receptors, we carried out the binding of [H-3]-dihydroalprenolol ([H-3]-DHA) to hippocampal membranes from rats deprived of REM sleep for 96 h. We also determined the binding of [H-3]-DHA to brainstem membranes, a brain region where noradrenergic nuclei are located. Rats were deprived of REM sleep using a water tank with multiple small platforms. [H-3-DHA] saturation conditions (concentrations ranging from 0.15 to 6 nM) were obtained in a crude ...
TY - JOUR. T1 - Alpha-1-adrenergic receptors in heart failure. T2 - The adaptive arm of the cardiac response to chronic catecholamine stimulation. AU - Jensen, Brian C.. AU - OConnell, Timothy D.. AU - Simpson, Paul C.. PY - 2014/4. Y1 - 2014/4. N2 - Alpha-1-adrenergic receptors (ARs) are G protein-coupled receptors activated by catecholamines. The alpha-1A and alpha-1B subtypes are expressed in mouse and human myocardium, whereas the alpha-1D protein is found only in coronary arteries. There are far fewer alpha-1-ARs than beta-ARs in the nonfailing heart, but their abundance is maintained or increased in the setting of heart failure, which is characterized by pronounced chronic elevation of catecholamines and beta-AR dysfunction. Decades of evidence from gain and loss-of-function studies in isolated cardiac myocytes and numerous animal models demonstrate important adaptive functions for cardiac alpha-1-ARs to include physiological hypertrophy, positive inotropy, ischemic preconditioning, and ...
1. Ten patients with essential hypertension received an intravenous load of hyperosmotic saline before and during treatment with propranolol. In seven patients blood pressure was lowered by the drug.. 2. In the control period saline infusion induced a sharp rise in cardiac output due to an increase in stroke volume. This pattern was absent during beta-adrenergic blockade. Renal blood flow showed a moderate rise in the control studies; this rise was not reduced during treatment. Natriuresis was reduced by propranolol.. 3. Measurements of central blood volume and central venous pressure in five patients revealed that modified responses during beta-adrenergic blockade may be due to a reduced venous return rather than to myocardial depression. ...
Defibrotide is a polydeoxyribonucleotide of mammalian origin which possesses profibrinolytic effect and PGI2-releasing capacity. Because of these properties, defibrotide has antithrombotic effects which are demonstrated in various experimental models
Mechanism of Action: ProAmatine® forms an active metabolite, desglymidodrine, that is an alpha1-agonist, and exerts its actions via activation of the alpha-adrenergic receptors of the arteriolar and venous vasculature, producing an increase in vascular tone and elevation of blood pressure. Desglymidodrine does not stimulate cardiac beta-adrenergic receptors. Desglymidodrine diffuses poorly across the blood-brain barrier, and is therefore not associated with effects on the central nervous system.. Administration of ProAmatine® results in a rise in standing, sitting, and supine systolic and diastolic blood pressure in patients with orthostatic hypotension of various etiologies. Standing systolic blood pressure is elevated by approximately 15 to 30 mmHg at 1 hour after a 10-mg dose of midodrine, with some effect persisting for 2 to 3 hours. ProAmatine® has no clinically significant effect on standing or supine pulse rates in patients with autonomic failure.. Pharmacokinetics:ProAmatine® is a ...