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Gotowe bibliografie tematyczne / Beta adrenergic receptor blockaders

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Gotowa bibliografia na temat „Beta adrenergic receptor blockaders”

Autor: Grafiati

Data publikacji: 4 czerwca 2021

Data aktualizacji: 21 lutego 2023

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Artykuły w czasopismach na temat "Beta adrenergic receptor blockaders"

1

DiCarlo, S. E., R. W. Blair, V. S. Bishop, and H. L. Stone. "Role of beta 2-adrenergic receptors on coronary resistance during exercise." Journal of Applied Physiology 64, no. 6 (June 1, 1988): 2287–93. http://dx.doi.org/10.1152/jappl.1988.64.6.2287.

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The effects of regional alpha- and specific beta 2-adrenergic receptor blockade on measurements of late diastolic coronary resistance (LDCR) and mean coronary blood flow velocity (CBFV) during exercise were examined in 14 conscious adult mongrel dogs. Specific beta 2-adrenergic receptor blockade (ICI 118.551) significantly decreased CBFV and increased LDCR by blockade of beta 2-vasodilator tone independent of alpha-adrenergic receptor-mediated tone and independent of altering myocardial metabolism. alpha-Adrenergic receptor blockade (phentolamine, 1 mg) significantly increased CBFV and decreased LDCR by blocking sympathetically mediated vasoconstrictor tone. There was no significant difference in the magnitude of response between alpha- and beta 2-adrenergic receptor blockade. These results demonstrate that alpha- and beta 2-adrenergic receptors have a significant and evidently equal influence on CBFV and LDCR during exercise. Four weeks of daily exercise and left stellate ganglionectomy (LSGx) prevented phentolamine-induced vasodilation but not ICI 118.551-induced vasoconstriction. This suggests that daily exercise and LSGx significantly decreased the alpha-adrenergic receptor-mediated vasoconstrictor tone on the coronary circulation, resulting in an apparently greater role for the coronary vascular beta 2-adrenergic receptor on the control of CBFV and LDCR during exercise.

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Awad, E. W., and M. Anctil. "IDENTIFICATION OF beta-LIKE ADRENOCEPTORS ASSOCIATED WITH BIOLUMINESCENCE IN THE SEA PANSY RENILLA KOELLIKERI." Journal of Experimental Biology 177, no. 1 (April 1, 1993): 181–200. http://dx.doi.org/10.1242/jeb.177.1.181.

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Previous studies have reported pharmacological and biochemical evidence for the involvement of adrenergic substances in the regulation of neuroeffector activities in the bioluminescent cnidarian Renilla koellikeri (Cnidaria, Anthozoa). Therefore, direct radiobinding assays were developed to identify and characterize beta-adrenergic binding in membrane preparations from this species, using the two beta-antagonists [3H]dihydroalprenolol and [3H]CGP12177 as tracers. In addition, the effect of various beta-adrenergic agents on luminescence was examined. Binding of the radioligands at 25°C was rapid, reversible, saturable and specific. Saturation studies revealed the presence of two different and independent classes of binding site, site1 and site2, in the body of the colony (rachis). In contrast, homogeneous populations of binding sites corresponding to site1 were detected in autozooid polyps and to site2 in the peduncle. The pharmacological profile of beta-adrenergic binding in R. koellikeri membrane preparations displayed properties consistent with the presence of two sites and followed a pattern similar to beta2- and beta1-adrenergic receptor subtypes for site1 and site2, respectively. Bioluminescence in polyps was induced by beta-agonists as well as by one beta1-selective antagonist, atenolol, and was blocked by several beta-blockers including (+/−)CGP12177. The specificity pattern of the physiological effect of beta-adrenergic drugs on luminescence mirrors that of the radioligand interaction with site1. This suggests that radioligand binding to site1 represents binding to the receptor that mediates luminescence excitation in R. koellikeri. Blockade of the luminescent responses to site1 agonists by isotonic MgCl2 indicates that this beta-adrenergic mechanism must rely on interneuronal transmission. Collectively, these results suggest the evolutionary conservation of beta-adrenoceptors and of their dual character from coelenterates to higher vertebrates.

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Jasper, J. R., H. J. Motulsky, L. C. Mahan, and P. A. Insel. "Beta-adrenoceptor metabolism in wild-type, Gs, and protein kinase A-variant S49 cells." American Journal of Physiology-Cell Physiology 259, no. 1 (July 1, 1990): C41—C46. http://dx.doi.org/10.1152/ajpcell.1990.259.1.c41.

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To determine the role of the stimulatory guanine nucleotide-binding protein, Gs, and adenosine 3',5'-cyclic monophosphate (cAMP)-dependent protein kinase in the basal metabolism of beta-adrenergic receptors in S49 lymphoma cells, we measured the return of receptor number and function after irreversible blockade of receptors. After inactivation of receptors with the irreversible ligand N8-(bromoacetyl)-N'-[3-(4-indolyoxy)-2-hydroxypropyl]-(2)-1,8-diam ino-p- methane (BIM), beta-adrenergic receptors (defined as [125I]iodocyanopindolol binding sites) reappeared in a biphasic manner, the faster phase having a half-time (t 1/2) of 3-8 h (approximately 50% of the sites) and the slower phase greater than 40 h. Although the slow phase is not readily explained, recovery of binding sites during the first 10 h matched recovery of receptor function after BIM treatment (as measured by stimulation of cAMP accumulation) and recovery of receptor sites after downregulation induced by the agonist isoproterenol. Thus quantifying receptor recovery during the first 10 h after BIM treatment appears to be a reasonable method for examining basal receptor metabolism in S49 cells. Measured in this way, metabolism of beta-adrenergic receptors is very similar in wild-type S49 and the following variant clones: cyc- (absent Gs alpha), UNC and H21a (defective Gs alpha), and kin- (lacking cAMP-dependent protein kinase activity). Although previous data have demonstrated that agonist-promoted downregulation of beta-adrenergic receptors requires functional receptor-Gs coupling, the current data suggest that neither Gs nor cAMP-dependent protein kinase activity plays an important role in the regulation of basal metabolism of beta-adrenergic receptors.(ABSTRACT TRUNCATED AT 250 WORDS)

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Vatner, S. F., D. R. Knight, and T. H. Hintze. "Norepinephrine-induced beta 1-adrenergic peripheral vasodilation in conscious dogs." American Journal of Physiology-Heart and Circulatory Physiology 249, no. 1 (July 1, 1985): H49—H56. http://dx.doi.org/10.1152/ajpheart.1985.249.1.h49.

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Norepinephrine (NE) elicits alpha-adrenergic vasoconstriction and beta 1-adrenergic increases in heart rate and myocardial contractility. To determine whether NE can also elicit peripheral beta 1-adrenergic vasodilation, conscious dogs were studied after recovery from instrumentation for the measurement of cardiac output, arterial pressure, and left ventricular (LV) pressure and calculations of LV dP/dt and total peripheral resistance (TPR). NE, after pretreatment with hexamethonium and phentolamine, reduced mean arterial pressure 40 +/- 5% from 117 +/- 9 mmHg and TPR 60 +/- 5% from 0.058 +/- 0.007 mmHg X ml-1 X min and increased cardiac output 55 +/- 11% from 2,159 +/- 188 ml/min. beta 1-Adrenergic blockade with atenolol reversed the vasodilation induced by NE completely, while at this time isoproterenol was still able to reduce peripheral resistance further, by 67 +/- 7%, indicating that beta 2-adrenergic receptors were not blocked. Administration of phentolamine to intact dogs caused a fall in mean arterial pressure (23 +/- 5%) and TPR (34 +/- 5.4%) and an endogenous increase in plasma NE (2,987 +/- 905 pg/ml) and epinephrine (584 +/- 92 pg/ml). These increases in cardiac output and decreases in TPR were also reversed by atenolol (0.5 mg/kg). Moreover, this dose of atenolol blocked the increases in iliac blood flow induced by local injection of NE in the limb. Thus, in the presence of alpha-adrenergic receptor blockade, either administration of NE or release of endogenous NE elicits potent peripheral vasodilation, which appears to involve a beta 1-adrenergic receptor mechanism.

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Kagiya, T., M. Hori, K. Iwakura, K. Iwai, Y. Watanabe, S. Uchida, H. Yoshida, A. Kitabatake, M. Inoue, and T. Kamada. "Role of increased alpha 1-adrenergic activity in cardiomyopathic Syrian hamster." American Journal of Physiology-Heart and Circulatory Physiology 260, no. 1 (January 1, 1991): H80—H88. http://dx.doi.org/10.1152/ajpheart.1991.260.1.h80.

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We investigated serial changes in myocardial norepinephrine content and myocardial adrenergic receptors during the development of cardiomyopathy in Syrian hamsters (Bio 14.6) and their age-matched healthy controls. We also examined phosphatidylinositide hydrolysis after alpha 1-adrenergic stimulation and the effects of alpha 1-blockade. We found that in the prehypertrophic stage, myocardial norepinephrine content and densities of alpha 1- and beta-adrenergic receptors were significantly higher in the cardiomyopathic hamsters than in the controls. However, in the early heart failure stage, beta-receptor density was 28% lower than that of the age-matched controls, although alpha 1-receptor density remained 55% higher. Norepinephrine-stimulated phosphatidylinositide hydrolysis in the cardiomyopathic hamster in the hypertrophic stage was twice that in the controls, indicating that the increase in alpha 1-adrenergic receptors is coupled with the intracellular signal transduction. Furthermore, selective alpha 1-adrenoceptor blockade by bunazosin in the cardiomyopathic hamsters from 70 to 170 days of age reduced myocardial hypertrophy and focal myocardial necrosis. Thus we conclude that increased alpha 1-adrenergic activity plays an important role in progression of cardiac hypertrophy is cardiomyopathic Syrian hamsters.

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Borst, M. M., R. Marquetant, W. Kubler, and R. H. Strasser. "Beta-blockade reduces effects of adenosine and carbachol by transregulation of inhibitory receptors and Gi proteins." American Journal of Physiology-Heart and Circulatory Physiology 272, no. 4 (April 1, 1997): H1672—H1679. http://dx.doi.org/10.1152/ajpheart.1997.272.4.h1672.

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Chronic blockade of stimulatory beta-adrenergic receptors may decrease inhibitory receptors of the adrenergic signal transduction system. This transregulation process might reduce the negative inotropic response of the myocardium to inhibitory receptor stimulation. Rats were treated for 6 days with the beta-blocker atenolol (2 mg/day). beta-Adrenergic receptors in cardiac plasma membranes increased from 49 +/- 6 to 75 +/- 9 fmol/mg protein (means +/- SE; P = 0.053), whereas muscarinic M2 receptors decreased (155 +/- 15 vs. 105 +/- 10 fmol/mg protein; P < or = 0.05). Moreover, inhibitory G alpha(i) proteins were reduced by 36%. The functional responses of isolated hearts to inhibitory agonists after prestimulation with isoproterenol (3 nmol/l) were significantly blunted. The Ki value for the negative inotropic response of the maximal rise in developed left ventricular pressure (dP/dt(max)) to adenosine (0.1-100 micromol/l) increased from 5.9 +/- 1.7 to 24.0 +/- 2.5 micromol/l (P < or = 0.001). A similar rightward shift of the dose-response curve was observed for the effects of adenosine on developed left ventricular pressure (LVP) and of carbachol (0.01-10 micromol/l) on LVP and dP/dt. Thus chronic beta-blockade leads to a coordinate transregulation of inhibitory receptors and Gi proteins, reducing the effects of inhibitory receptor activation of the heart. This mechanism may contribute to the beneficial effects of beta-blocker therapy in heart failure.

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Kaufman, Beth D., and Robert E. Shaddy. "Beta-adrenergic receptor blockade and pediatric dilated cardiomyopathy." Progress in Pediatric Cardiology 24, no. 1 (November 2007): 51–57. http://dx.doi.org/10.1016/j.ppedcard.2007.08.004.

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Laughlin, M. H., and R. B. Armstrong. "Adrenoreceptor effects on rat muscle blood flow during treadmill exercise." Journal of Applied Physiology 62, no. 4 (April 1, 1987): 1465–72. http://dx.doi.org/10.1152/jappl.1987.62.4.1465.

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The purpose of this study was to examine the effects of the adrenergic receptors on the distribution of blood flow within and among skeletal muscles in rats. Blood flow was measured with the radiolabeled microsphere technique before exercise and during treadmill exercise at 15 or 60 m/min. Alpha- (phentolamine) or beta- (propranolol) adrenergic blocking drugs were administered, and then blood flow was measured and results compared with those from saline-treated rats. Before exercise, alpha-blockade caused increases in total muscle blood flow and in all fast-twitch muscles, whereas muscles composed of greater than 20% slow-twitch fibers showed no effect. During exercise at 15 m/min, the normal increase in total muscle blood flow was attenuated by alpha-blockade. Compared with controls, blood flow was less in the high-oxidative (fast and slow) muscle fiber areas of extensor muscles, whereas blood flow to white areas of extensor muscles was increased. beta-Blockade tended to decrease muscle blood flow before exercise and during exercise at 15 m/min with no apparent relationship between the effects of blockade on blood flow and muscle fiber type. These effects of beta-blockade were not apparent during exercise at 60 m/min. We conclude that before exercise alpha-receptor effects are limited to fast muscle, whereas beta-receptor influences are independent of fiber type, beta-receptors contribute to the initial hyperemia of exercise at 15 m/min, and beta-receptor influence is inversely related to metabolic rate.

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Kuleshova, E. V., N. V. Kuzmenko, M. G. Pliss, and V. A. Tsyrlin. "Mechanisms of beta-blockers antihypertensive action." "Arterial’naya Gipertenziya" ("Arterial Hypertension") 27, no. 3 (August 4, 2021): 291–99. http://dx.doi.org/10.18705/1607-419x-2021-27-3-291-299.

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This article presents an analysis of data on the mechanisms of antihypertensive effect of β-adrenergic receptor blockers. The article describes the effectiveness of cardiotropic action of drugs to reduce high blood pressure (BP) with short-term and long-term action of compounds, the effect of blockers on the activity of plasma renin. The inﬂuence of β-blockers on the central mechanisms of blood circulation regulation is considered. Information on the effect of β-blockers on myogenic mechanisms of vascular tone regulation is presented. The possibilities of blockade of β-adrenergic receptors of endothelium-dependent hyperpolarization of smooth muscles of resistive arteries, violation of the NO-cGMP pathway and blockade of Ca2+ channel currents as factors providing expansion of resistive vessels and reduction of high BP are analyzed.

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Ferrara, L. Aldo, Teodoro Marotta, Paolo Rubba, Biagio De Simone, Giovanni Leccia, Stefano Soro, and Mario Mancini. "Effects of alpha-adrenergic and beta-adrenergic receptor blockade on lipid metabolism." American Journal of Medicine 80, no. 2 (February 1986): 104–8. http://dx.doi.org/10.1016/0002-9343(86)90168-3.

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Rozprawy doktorskie na temat "Beta adrenergic receptor blockaders"

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Plank, David Michael. "Calcium dynamics, β-adrenergic receptor blockade, and cardiac function in failing and non-failing hearts". University of Cincinnati / OhioLINK, 2003. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1053431441.

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Plank, David M. "Calcium dynamics, [beta]-adrenergic receptor blockade, and cardiac function in failing and non-failing hearts." Cincinnati, Ohio : University of Cincinnati, 2003. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=ucin1053431441.

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Grogan, Shawn Patrick, of Western Sydney Hawkesbury University, Faculty of Environmental Management and Agriculture, and School of Agriculture and Rural Development. "Endocrine alteration of meat quality and gene expression in rats and deer." THESIS_FEMA_ARD_Grogan_S.xml, 1998. http://handle.uws.edu.au:8081/1959.7/724.

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Stress activates a number of endocrine pathways that alter an animal's physiology in a manner which can result in undesirable meat quality. Animals frequently exhibit meat quality defects, including ecchymosis, at slaughter due to the stress of slaughter. This thesis explores how stress related hormones interact with adrenergic receptors to alter muscle and vascular physiology. Fallow deer were exposed to either a transciptional regulator (hydrocortisone), a beta adrenergic recptor agonist (clenbuterol) or a beta adrenergic receptor antagonist (propranolol). The administration of hydrocortisone resulted in a negative feed-back type reduction in circulating cortisol. Animals treated with propranolol and clenbuterol displayed less severe eccymosis. These results indicated that the beta 2 adrenergic receptor (B2AR) is important in controlling ecchymosis severity. B2AR was also found to be important in mediating vascular dynamics, growth and energy pathways. To investigate how adrenergic receptors alter skeletal muscle gene expression and meat quality, an in vivo wistar rat model was developed in conjunction with in vitro muscle cell (L6) experiments. Gene expression of B2AR, its associated kinase (BARK) and collagen type III, prolyl- 4-hydroxylase (P4Hy) was measured in rat muscle and L6 cells. Following exposure to clenbuterol and hydrocortisone, growth and meat quality were determined. The L6 experiments revealed that gene expression following exposure to hydrocortisone and B2AR ligands paralleled the in vivo rat changes in B2AR, BARK, collagen type III, and P4Hy gene expression. In both L6 and wistar rat models the B2AR and BARK genes are similarly expressed following clenbuterol exposure. Both rats and deer exposed to clenbuterol had significant increases in growth rate and a reduction of intramuscular fat. The B2AR therefore appears to be a major mediator of many interrelated events including energy distribution, growth and vascular response to stress. Habituating animals to stress stimuli may increase their coping ability and improve welfare and meat quality.<br>Doctor of Philosophy (PhD)

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Grogan, Shawn Patrick. "Endocrine alteration of meat quality and gene expression in rats and deer." Thesis, [Richmond, N.S.W.] : CSIRO Animal Production : School of Agriculture, University of Western Sydney, Hawkesbury, 1998. http://handle.uws.edu.au:8081/1959.7/724.

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Stress activates a number of endocrine pathways that alter an animal's physiology in a manner which can result in undesirable meat quality. Animals frequently exhibit meat quality defects, including ecchymosis, at slaughter due to the stress of slaughter. This thesis explores how stress related hormones interact with adrenergic receptors to alter muscle and vascular physiology. Fallow deer were exposed to either a transciptional regulator (hydrocortisone), a beta adrenergic recptor agonist (clenbuterol) or a beta adrenergic receptor antagonist (propranolol). The administration of hydrocortisone resulted in a negative feed-back type reduction in circulating cortisol. Animals treated with propranolol and clenbuterol displayed less severe eccymosis. These results indicated that the beta 2 adrenergic receptor (B2AR) is important in controlling ecchymosis severity. B2AR was also found to be important in mediating vascular dynamics, growth and energy pathways. To investigate how adrenergic receptors alter skeletal muscle gene expression and meat quality, an in vivo wistar rat model was developed in conjunction with in vitro muscle cell (L6) experiments. Gene expression of B2AR, its associated kinase (BARK) and collagen type III, prolyl- 4-hydroxylase (P4Hy) was measured in rat muscle and L6 cells. Following exposure to clenbuterol and hydrocortisone, growth and meat quality were determined. The L6 experiments revealed that gene expression following exposure to hydrocortisone and B2AR ligands paralleled the in vivo rat changes in B2AR, BARK, collagen type III, and P4Hy gene expression. In both L6 and wistar rat models the B2AR and BARK genes are similarly expressed following clenbuterol exposure. Both rats and deer exposed to clenbuterol had significant increases in growth rate and a reduction of intramuscular fat. The B2AR therefore appears to be a major mediator of many interrelated events including energy distribution, growth and vascular response to stress. Habituating animals to stress stimuli may increase their coping ability and improve welfare and meat quality.

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Bagley, John Sorrell. "The beta adrenergic receptor in septic shock." Thesis, University of Aberdeen, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.305466.

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The myocardial depression found during septic shock has been a subject of intense study for many years. Many theories exist as to the precise cause of this condition but in this thesis the role of the β-adrenergic receptor is examined. Some investigators have found reduced response to β-adrenergic stimulation in models of septic shock in animals. This is of interest to the clinician since adrenergic stimulation is a key manipulation in the management of septic shock. An animal model of septic shock was established using a comparatively small dose of <i>Escherichia coli</i> endotoxin infused into the male Sprague-Dawley rat. Heart function and response to isoprenaline, a β1-agonist, were measured in an <i>in vitro</i> organ bath. A reduction in the force of contraction was found together with a shift in the response curve to the right. These findings were associated with an increase in the number of β-receptors in the ventricular tissue from the same hearts, a measurement made using radioligand binding with I<sup>125</sup>-(-)-Iodocyanopindolol, a β1-antagonist. The finding of more β-receptors in the context of septic shock raises interesting questions discussed in the thesis. When forskolin, a plant alkaloid that stimulates the adenyl cyclase enzyme, was used to stimulate the atria <i>in vitro</i> the same response was found in the endotoxin treated and the normal groups. This is strong evidence that endotoxin causes a myocardial depressant effect mediated prior to adenylcyclase in the β-receptor transduction cascade.

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Higgins, Thomas John Diatchenko Luda. "Molecular characterization of [beta]2 adrenergic receptor haplotypes." Chapel Hill, N.C. : University of North Carolina at Chapel Hill, 2008. http://dc.lib.unc.edu/u?/etd,1602.

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Thesis (M.S.)--University of North Carolina at Chapel Hill, 2008.<br>Title from electronic title page (viewed Sep. 16, 2008). "... in partial fulfillment of the requirements for the degree of Master's of Science in the Curriculum in Neurobiology." Discipline: Neurobiology; Department/School: Medicine. On title page, [beta] appers as Greek character and 2 appears in subscript.

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Vincent, Karla Kristine. "Transactivation of Beta 2 Adrenergic Receptor by Bradykinin type 2 Receptor via heterodimerization." Diss., Georgia Institute of Technology, 2009. http://hdl.handle.net/1853/37117.

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Although a long standing convention maintained that G Protein Coupled Receptors (GPCRs) exist in the plasma membrane solely as monomers, substantial work over the last two decades has demonstrated that these ubiquitous receptors can and in many cases, preferentially, exist as homodimers, heterodimers, or higher order oligomers. Often, two GPCRs of the same class heterodimerize; it is less common for two GPCRs of different signaling pathways to interact. The work presented here studied the physical and functional interaction of two GPCRs from discrete classes, the Beta 2 Adrenergic Receptor (β2AR), a Gαs-coupled receptor, and Bradykinin type 2 Receptor (Bk2R), a Gαq coupled receptor. These data show that Bk2R and β2AR are physically coupled when heterologously expressed in Xenopus oocytes, and in pheochromocytoma (PC12) cells and in freshly isolated murine ventricular myocytes, two systems that endogenously express these receptors. This physical coupling led to functional consequences in heterologous and endogenous expression systems, as Bk2R was able to transactivate β2AR signaling via its direct interaction with the receptor. Furthermore, coexpression of Bk2R shifted the dose response curve of β2AR for its selective agonist rightward in Xenopus oocyte electrophysiology experiments, suggesting the presence of Bk2R negatively affected β2AR native pharmacology. Up to thirty minutes of either bradykinin (BK) or isoproterenol exposure did not change the relative amount of Bk2R/β2AR heterodimer in PC12 cells, a rat adrenal medulla tumor cell line that endogenously expresses these receptors. Despite the obvious signaling consequences, the Bk2R/β2AR heterodimer accounted for only 10% of the total β2AR protein detected and 20% of the total Bk2R protein detected. When other Bk2R-specific ligands were also tested to examine the extent of β2AR transactivation, our data showed that both Lys-des-Arg-Bradykinin, a Bk2R partial agonist and NPC 567, a Bk2R antagonist, transactivated β2AR to the same extent as BK. Taken together, our data provide a novel mode of receptor regulation and signaling via Bk2R/β2AR heterodimerization. Because a large percentage of therapeutics target GPCRs, a greater understanding of how a GPCR heterodimer functions could be beneficial for targeting new drugs and refining existing drugs. Understanding the Bk2R/β2AR heterodimer provides a new perspective on the myriad of fucntional consequences that occur when a GPCR is activated.

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Snyder, Ellen Amanda Flood Patrick M. "[beta]2-adrenergic receptor modulation of macrophage inflammatory mediator production." Chapel Hill, N.C. : University of North Carolina at Chapel Hill, 2007. http://dc.lib.unc.edu/u?/etd,1344.

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Thesis (M.S.)--University of North Carolina at Chapel Hill, 2007.<br>Title from electronic title page (viewed Apr. 25, 2008). "... in partial fulfillment of the requirements for the degree of Master of Science in the Curriculum of Oral Biology." Discipline: Oral Biology; Department/School: Dentistry. On title page, [beta] appears as Greek character and 2 appears as subscript.

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Robson, Alice. "In vitro reconstitution and stability of a beta-adrenergic receptor." Thesis, University of Bristol, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.424005.

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Zolty, Ronald. "Beta 1 and Alpha 2C adrenergic receptor polymorphisms and response to beta blockers in heart failure patients /." Connect to full text via ProQuest. Limited to UCD Anschutz Medical Campus, 2007.

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Thesis (Ph.D. in Clinical Science) -- University of Colorado Denver, 2007.<br>Typescript. Includes bibliographical references (leaves 130-142). Free to UCD affiliates. Online version available via ProQuest Digital Dissertations;

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Książki na temat "Beta adrenergic receptor blockaders"

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Cruickshank, J. M. Beta-blockers in clinical practice. Edinburgh: Churchill Livingstone, 1988.

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Prichard, Brian N. C. 1932-, ed. Beta-blockers in clinical practice. Edinburgh: Churchill Livingstone, 1987.

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Drugs looking for diseases: Innovative drug research and the development of the beta blockers and the calcium antagonists. Dordrecht: Kluwer Academic Publishers, 1991.

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Advances in adrenergic receptor biology. Amsterdam: Elsevier, 2011.

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Owens, Helen. The effect of beta-adrenergic receptor antagonists on the temporal accommodative response. Birmingham: Aston University. Department of Vision Sciences, 1991.

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1944-, Costello J. F., and Mann Ronald D. 1928-, eds. Beta agonists in the treatment of asthma: The proceedings. Carnforth, Lancs, UK: Parthenon Pub. Group, 1992.

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Richard, Beasley, and Pearce Neil, eds. The Role of beta receptor agonist therapy in asthma mortality. Boca Raton: CRC Press, 1993.

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1946-, Frishman William H., ed. Beta₃-adrenergic agonism: A new concept in human pharmacotherapy. Armonk, N.Y: Futura, 1995.

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Cruickshank, J. M. Beta-Blockers in Clinical Practice. 2nd ed. W.B. Saunders Company, 1994.

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1948-, Deedwania Prakash C., ed. Beta-blockers and cardiac arrhythmias. New York: M. Dekker, 1992.

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Części książek na temat "Beta adrenergic receptor blockaders"

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Schomburg, Dietmar, and Dörte Stephan. "beta-Adrenergic-receptor kinase." In Enzyme Handbook, 113–17. Berlin, Heidelberg: Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-642-59025-2_21.

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Ross, Elliott M. "Reconstitution of the Beta-Adrenergic Receptor and Its Biochemical Functions." In The Beta-Adrenergic Receptors, 125–79. Totowa, NJ: Humana Press, 1991. http://dx.doi.org/10.1007/978-1-4612-0463-3_4.

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Erhardt, Paul W., and Lajos Matos. "Selective Beta-Adrenergic Receptor-Blocking Agents." In Analogue-based Drug Discovery, 193–232. Weinheim, FRG: Wiley-VCH Verlag GmbH & Co. KGaA, 2006. http://dx.doi.org/10.1002/3527608001.ch11.

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Stiles, Gary L. "Drug and Hormonal Regulation of the Beta-Adrenergic Receptor—Adenylate Cyclase System." In The Beta-Adrenergic Receptors, 345–86. Totowa, NJ: Humana Press, 1991. http://dx.doi.org/10.1007/978-1-4612-0463-3_8.

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Özkaya, Esen, and Kurtuluş Didem Yazganoğlu. "Beta Adrenergic Receptor Blockers (Class II Antiarrhythmics)." In Adverse Cutaneous Drug Reactions to Cardiovascular Drugs, 111–21. London: Springer London, 2014. http://dx.doi.org/10.1007/978-1-4471-6536-1_6.

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Hershberger, Ray E. "Beta-Adrenergic Receptor Agonists and Antagonists in Heart Failure." In Congestive Heart Failure, 454–92. New York, NY: Springer New York, 1994. http://dx.doi.org/10.1007/978-1-4613-8315-4_25.

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Hammond, J., and J. L. Balligand. "Signalling Microdomains: The Beta-3 Adrenergic Receptor/NOS Signalosome." In Microdomains in the Cardiovascular System, 215–44. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-54579-0_11.

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Collins, Sheila, and S. Wang. "Molecular regulation of the β2-adrenergic receptor by long- and short-acting β-agonists." In Treatment of Asthma: The long-acting beta-2-agonists, 1–14. Vienna: Springer Vienna, 1998. http://dx.doi.org/10.1007/978-3-7091-7513-2_1.

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Davideit, Hanna, Annekathrin Haberland, Sabine Bartel, Sarah Schulze-Rothe, Johannes Müller, and Katrin Wenzel. "Determination of Agonistically Acting Autoantibodies to the Adrenergic Beta-1 Receptor by Cellular Bioassay." In Autoantibodies, 95–102. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-8949-2_8.

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Kather, H. "Beta Adrenergic Receptor Mediated Stimulation of Adenine Nucleotide Catabolism and Purine Release in Human Adipocytes." In Purines in Cellular Signaling, 120–25. New York, NY: Springer New York, 1990. http://dx.doi.org/10.1007/978-1-4612-3400-5_20.

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Streszczenia konferencji na temat "Beta adrenergic receptor blockaders"

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Cano, E. J., J. A. Gonzalez, J. L. Perez-Lara, F. Casado, A. Zhang, and C. Zeana. "Beta-Adrenergic Receptor Blockers in E. coli Bacteremia: Severity of Presentation and Outcomes." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a6499.

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Carroll, Christopher L., Craig Schramm, Indira Sadhu, and Aaron R. Zucker. "Beta-Adrenergic Receptor Haplotype Associated With Recurrent Near Fatal Asthma Exacerbations In Children." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a2509.

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Khan, Y., SJ Fowler, and G. Tavernier. "S140 Beta-2-adrenergic receptor gene polymorphisms in severe asthma: a systematic review." In British Thoracic Society Winter Meeting, Wednesday 17 to Friday 19 February 2021, Programme and Abstracts. BMJ Publishing Group Ltd and British Thoracic Society, 2021. http://dx.doi.org/10.1136/thorax-2020-btsabstracts.145.

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Kim, Joon H., Lawrence D. Longo, and Sean M. Wilson. "Attenuated Beta Adrenergic Receptor Mediated Pulmonary Vasodilation In High Altitude Term-Fetal Sheep." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a4831.

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Ou, Z., L. Wang, X. Hong, Z. Shen, and Z. Shao. "Overexpression or Lack of beta 2-Adrenergic Receptor Correlate with Progression of Breast Cancer." In Abstracts: Thirty-Second Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 10‐13, 2009; San Antonio, TX. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-09-4165.

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Stolk, R., E. van der Pasch, F. Naumann, J. Schouwstra, T. van Herwaarden, J. Gerretsen, R. Schambergen, et al. "Anti-Inflammatory Effects of Phenylephrine in Mice and Humans Mediated via the Beta Adrenergic Receptor." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a2590.

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Zucker, Aaron R., Christopher L. Carroll, Indira Sadhu, and Craig Schramm. "Racial Differences Of Beta-Adrenergic Receptor Genotypes In Children Hospitalized For Near Fatal Asthma Exacerbations." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a3907.

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Carroll, Christopher L., Aaron R. Zucker, Kathleen Sala, and Craig M. Schramm. "Racial Differences Of Beta-Adrenergic Receptor Genotype & Response To Therapy In Children With Bronchiolitis." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a4164.

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Dong, Junhong, Ping Wang, Qingluan Xu, Kunpeng Lv, Yu Wang, and Junhong Dong. "Expression of Beta-Adrenergic Receptor in Glioma LN229 Cells and Its Effect on Cell Proliferation." In 2016 7th International Conference on Education, Management, Computer and Medicine (EMCM 2016). Paris, France: Atlantis Press, 2017. http://dx.doi.org/10.2991/emcm-16.2017.140.

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Owens, H., B. Winn, B. Gilmartin, and J. R. Pugh. "The Effect of a Topical Beta-Adrenergic Receptor Antagonist on the Dynamics of Steady-State Accommodation." In Noninvasive Assessment of the Visual System. Washington, D.C.: Optica Publishing Group, 1991. http://dx.doi.org/10.1364/navs.1991.md9.

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Streszczenie:

Temporal fluctuations in the steady-state human ocular accommodation response are characterised by two principal frequency components: a high frequency component (HFC: 1-2.2Hz) and a low frequency component (LFC:<0.5Hz) (Campbell, Robson and Westheimer, 1959; Kotulak and Schor, 1986; Winn et al, 1989). Recent work has demonstrated that the location of the HFC is significantly correlated with arterial pulse (Winn et al, 1990). These findings have led to the proposal that the HFCs are not governed by an accommodative control system, although they may potentially be utilised in conjunction with the LFCs by a sensory detection system which monitors retinal image contrast during steady-state accommodation. Further, HFCs could provide a useful non-invasive technique for investigating the ocular consequences of arterial pulse (AP).

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