Готові списки джерел за темами / Endothelin receptor

Добірка наукової літератури з теми "Endothelin receptor"

Автор: Grafiati
Опубліковано: 31 січня 2023

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Статті в журналах з теми "Endothelin receptor":

1

Saenz de Tejada, I., M. P. Carson, A. de las Morenas, I. Goldstein, and A. M. Traish. "Endothelin: localization, synthesis, activity, and receptor types in human penile corpus cavernosum." American Journal of Physiology-Heart and Circulatory Physiology 261, no. 4 (October 1, 1991): H1078—H1085. http://dx.doi.org/10.1152/ajpheart.1991.261.4.h1078.

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The localization, synthesis, and activity of endothelin and the receptor types mediating its effects in penile corpus cavernosum were investigated in whole tissue and in cultured cells derived from this tissue. With immunocytochemistry, utilizing an antiendothelin 1 (ET-1) monoclonal antibody, endothelin-like immunoreactivity was localized intensely in the endothelium and to a lesser degree in the trabecular smooth muscle. Human corpus cavernosum endothelial cells in culture expressed preproendothelin 1 mRNA, as determined by Northern blot analysis. Significant amounts of endothelin-like immunoreactivity were measured by radioimmunoassay in the supernatants of corpus cavernosum endothelial cells in culture. Endothelins are potent constrictors and caused long-lasting contractions of corporeal strips in organ chambers. Equilibrium binding analysis of endothelins to their receptor sites revealed high-affinity, specific, and saturable binding of labeled endothelins to corporeal membranes. Competition binding experiments demonstrated receptors with high affinity for ET-1 and -2 and low affinity for ET-3 and another, less abundant, set of receptors with high affinity for ET-1, -2, and -3. Affinity labeling of endothelins to corporeal membranes, followed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis analysis, revealed that ET-1 and -2 cross-linked specifically to three different molecular mass components (75, 52, and 34 kDa). ET-3 bound only to the 34-kDa component. It is concluded that human corpus cavernosum endothelium has the ability to synthesize and release endothelin, that endothelins contract corporeal smooth muscle, and that at least two distinct endothelin receptors may exist and are differentiated by their affinity for ET-3.
2

Barton, Matthias, and Masashi Yanagisawa. "Endothelin: 30 Years From Discovery to Therapy." Hypertension 74, no. 6 (December 2019): 1232–65. http://dx.doi.org/10.1161/hypertensionaha.119.12105.

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Discovered in 1987 as a potent endothelial cell–derived vasoconstrictor peptide, endothelin-1 (ET-1), the predominant member of the endothelin peptide family, is now recognized as a multifunctional peptide with cytokine-like activity contributing to almost all aspects of physiology and cell function. More than 30 000 scientific articles on endothelin were published over the past 3 decades, leading to the development and subsequent regulatory approval of a new class of therapeutics—the endothelin receptor antagonists (ERAs). This article reviews the history of the discovery of endothelin and its role in genetics, physiology, and disease. Here, we summarize the main clinical trials using ERAs and discuss the role of endothelin in cardiovascular diseases such as arterial hypertension, preecclampsia, coronary atherosclerosis, myocardial infarction in the absence of obstructive coronary artery disease (MINOCA) caused by spontaneous coronary artery dissection (SCAD), Takotsubo syndrome, and heart failure. We also discuss how endothelins contributes to diabetic kidney disease and focal segmental glomerulosclerosis, pulmonary arterial hypertension, as well as cancer, immune disorders, and allograft rejection (which all involve ET A autoantibodies), and neurological diseases. The application of ERAs, dual endothelin receptor/angiotensin receptor antagonists (DARAs), selective ET B agonists, novel biologics such as receptor-targeting antibodies, or immunization against ET A receptors holds the potential to slow the progression or even reverse chronic noncommunicable diseases. Future clinical studies will show whether targeting endothelin receptors can prevent or reduce disability from disease and improve clinical outcome, quality of life, and survival in patients.
3

Auguet, Michel, Sylvie Delaflotte, Pierre-Etienne Chabrier, and Pierre Braquet. "Characterization of endothelin receptors mediating contraction and relaxation in rabbit saphenous artery and vein." Canadian Journal of Physiology and Pharmacology 71, no. 10-11 (October 1, 1993): 818–23. http://dx.doi.org/10.1139/y93-122.

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The endothelin receptors in rabbit isolated rings of saphenous artery and saphenous vein have been characterized using endothelin-1, endothelin-2, endothelin-3, sarafotoxin S6c, and BQ123. Although artery rings were more sensitive than those from vein to the contractile action of phenylephrine, endothelin-1 was about three times more potent as a contractile agonist on vein than on artery. In rings precontracted with phenylephrine, carbachol was 10 times more potent in vein than in artery rings to induce endothelium-dependent relaxation. However, in rings precontracted to a similar tone by endothelin-1, the relaxation elicited by carbachol was reduced in the vein but remained unchanged in the artery. In endothelium-denuded saphenous artery, endothelin-1 and endothelin-2 elicited contraction with equal potency, whereas endothelin-3 and sarafotoxin S6c were weak agonists. In saphenous vein, the rank order of sensitivity was sarafotoxin S6c > endothelin-2 > endothelin-1 = endothelin-3, whereas sarafotoxin S6c and, to a lesser extent, endothelin-3 act as partial agonists. The ETA receptor antagonist BQ123 shifted, to the right, the concentration–response curves of endothelin-1 on endothelium-denuded saphenous artery (pA2 = 7.25). In the endothelium-denuded saphenous vein, 10 μM BQ123 shifted to the right only the response to high concentrations of endothelin-1. In vein but not in artery, endothelin-1 and sarafotoxin S6c induced an endothelium-dependent relaxation, which was increased, in the case of endothelin-1, in the presence of BQ123. These results indicate that the rabbit saphenous vein contains a mixed population of ETA and ETB vasoconstrictor receptors located in the smooth muscle cells and vasorelaxant ETB receptors situated on endothelial cells. In contrast, the saphenous artery only possesses smooth muscle cell ETA receptors responsible for constriction.Key words: endothelium, endothelin, vein, artery, BQ123.
4

Lüscher, Thomas F., and Matthias Barton. "Endothelins and Endothelin Receptor Antagonists." Circulation 102, no. 19 (November 7, 2000): 2434–40. http://dx.doi.org/10.1161/01.cir.102.19.2434.

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5

Nandagopal, Anitha, and Mubeen Unnisa Shamsia. "A REVIEW ON ENDOTHELINS: AN UPDATE." Asian Journal of Pharmaceutical and Clinical Research 11, no. 4 (April 1, 2018): 38. http://dx.doi.org/10.22159/ajpcr.2018.v11i4.23255.

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Endothelin (ET) is the most potent vasoconstrictor. It is secreted by the endothelial cells. At low concentration, it acts as an agonist for endothelium-derived relaxing factors and thereby causes vasodilatation, and at higher concentration it acts as a potent vasoconstrictor. It is synthesized by proteolytic cleavage of preproendothelin to proendothelin by the action of metallopeptidases and chymase, which is further cleaved into mature form of ET by endothelin converting enzyme. There are four isoforms of ET, namely, ET-1, ET-2, ET-3, and ET-4. ET acts on 2 types of receptors. Binding of ET-1 to ETA receptor at the vascular smooth muscle cells induces vasoconstriction. It also produces vasoconstriction by acting on the ETB2 receptor of vascular smooth muscle cells but promotes vasodilatation at ETB1 receptor present on the endothelial cell.
6

Barber, D. A., S. R. Michener, S. C. Ziesmer, and V. M. Miller. "Chronic increases in blood flow upregulate endothelin-B receptors in arterial smooth muscle." American Journal of Physiology-Heart and Circulatory Physiology 270, no. 1 (January 1, 1996): H65—H71. http://dx.doi.org/10.1152/ajpheart.1996.270.1.h65.

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Experiments were designed to characterize endothelin receptors in arteries after chronic increases in blood flow. A fistula was created between the femoral artery and vein in one hindlimb of dogs; contralateral blood vessels were sham operated. Sham- and fistula-operated arteries were removed 6 wk postoperatively. Some arteries were prepared for measurement of isometric force or for isolation of membrane proteins. Other arteries were used for histological staining with an endothelin-B (ETB) receptor antibody. In arteries suspended for the measurement of isometric force, endothelin-1 produced concentration-dependent increases in tension that were significantly greater in fistula- than in sham-operated arteries without endothelium. The ETB-receptor-selective peptide sarafotoxin S6c produced concentration-dependent increases in tension only in fistula-operated arteries. In receptor-binding studies of membrane proteins, Scatchard analysis of saturation binding with 125I-labeled endothelin-1 (125I-endothelin-1) indicated that the total number of receptors was greater in fistula-operated arteries; affinity was threefold less in fistula- than in sham-operated arteries. Competitive displacement of 125I-endothelin-1 by endothelin-3 was significant for a two-site model in membranes prepared from sham-and fistula-operated arteries. Competitive inhibition of 125I-endothelin-1 binding by sarafotoxin S6c was significant for a one-site binding model in all arteries. Sarafotoxin S6c binding sites were elevated significantly in fistula-operated arteries. Immunohistochemical staining for the ETB receptor was significantly greater in both the endothelium and smooth muscle of fistula- than in sham-operated arteries. These results suggest that chronic increases in blood flow upregulate endothelin receptors, including ETB receptors in arterial smooth muscle.
7

Hagiwara, H., T. Nagasawa, T. Yamamoto, K. M. Lodhi, T. Ito, N. Takemura, and S. Hirose. "Immunochemical characterization and localization of endothelin ETB receptor." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 264, no. 4 (April 1, 1993): R777—R783. http://dx.doi.org/10.1152/ajpregu.1993.264.4.r777.

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A highly specific antiserum was raised against purified bovine endothelin ETB receptor and used to determine the tissue distribution of the receptor subtype ETB and to localize the receptor immunohistochemically in the kidney, adrenal gland, lung, cerebellum, and pituitary gland whose functions are known to be under strong influence of endothelin. The antiserum raised in a rabbit specifically recognized the receptor band on Western blot analysis of membrane proteins. Furthermore, it immunoprecipitated only ETB, establishing its ETB specificity. By determination of the percentage of the total number of the endothelin receptors that is immunoprecipitable with the antiserum, the amounts of the ETB relative to those of the ET receptors were found to vary from tissue to tissue: lung (70%), cerebellum (55%), pituitary gland (50%), kidney (25%), adrenal gland (10%), and testis (< 2%). This means that, in the lung, ET is the major form, whereas in the testis, ETA is predominant, comprising >95% of the receptors. Immunohistochemical examination of tissue sections revealed endothelium localization of the ETB endothelin receptor.
8

Moreland, Suzanne. "Endothelin receptor antagonists: a brief review." Canadian Journal of Physiology and Pharmacology 72, no. 11 (November 1, 1994): 1469–71. http://dx.doi.org/10.1139/y94-212.

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The endothelins are a family of potent vasoconstrictors, some of which also have vasodilatory activity. In many diseases associated with tissue hypoxia or ischemia and in diseases in which vasoconstriction plays a role, the circulating levels of endothelin are higher than in healthy, control subjects. These findings stimulated research aimed at discovering endothelin receptor antagonists. This review focuses on the binding potency and vascular activity of these new peptide and nonpeptide endothelin receptor antagonists.Key words: endothelin, endothelin receptor subtypes, vascular smooth muscle, endothelin receptor antagonist.
9

Sakaguchi, H., M. Kozuka, S. Hirose, T. Ito, and H. Hagiwara. "Properties and localization of endothelin-1-specific receptors in rat testicles." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 263, no. 1 (July 1, 1992): R15—R18. http://dx.doi.org/10.1152/ajpregu.1992.263.1.r15.

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The characterization and localization of rat testicular endothelin receptors were studied. Receptor binding assay with radiolabeled members of the endothelin family revealed that endothelin-1-specific receptors were present in rat testes; a maximal binding capacity of 250 +/- 62 fmol/mg protein and a dissociation constant value of 0.35 +/- 0.06 nM were calculated from the Scatchard plot. The affinities for endothelin analogues were endothelin-1 = endothelin-2 much greater than endothelin-3 much greater big endothelin-1 for the membrane-bound receptors. Receptors of endothelin-1 were localized in peritubular myoid cells and interstitial cells of rat testis by 125I-labeled endothelin-1 autoradiography; the receptors were undetectable in spermatogenic cells. The presence of endothelin-1 receptors in the rat testis raises the possibility that one or more of the endothelins may play a physiological role in the regulation of testicular function.
10

Lankhorst, Stephanie, A. H. Jan Danser, and Anton H. van den Meiracker. "Endothelin-1 and antiangiogenesis." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 310, no. 3 (February 1, 2016): R230—R234. http://dx.doi.org/10.1152/ajpregu.00373.2015.

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Antiangiogenesis, targeting vascular endothelial growth factor (VEGF), has become a well-established treatment for patients with cancer. This treatment is associated with nitric oxide (NO) suppression and a dose-dependent activation of the endothelin system, resulting in preeclampsia-like features, particularly hypertension and renal injury. Studies in endothelium NO synthase (eNOS)-deficient mice and pharmacological treatment with endothelin receptor blockers and sildenafil indicate that an activated endothelin system, rather than NO suppression, mediates the side effects of angiogenesis inhibitors. Activation of the endothelin system is also observed in preeclamptic women, where it is related to the increased placental production of sFlt-1, the soluble form of the VEGF receptor-1. This receptor binds VEGF, thereby having the same consequences as antiangiogenic treatment with VEGF inhibitors. The side effects of antiangiogenic treatment in patients with cancer may be dose limiting, thereby impairing its therapeutic potential. In addition, because endothelin exerts proangiogenic effects, investigation of the effects of endothelin receptor blockade in patients with cancer treated with angiogenesis inhibitors is warranted.
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Статті в журналах Дисертації Книги

Дисертації з теми "Endothelin receptor":

1

Kelland, Nicholas. "The role of the endothelial cell endothelin B receptor in cardiovascular function." Thesis, University of Edinburgh, 2007. http://hdl.handle.net/1842/1899.

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Endothelin-1 (ET-1) binds to endothelin A (ETA) and B (ETB) receptors on vascular smooth muscle cells, resulting in profound vasoconstriction and cellular proliferation. In contrast, activation of endothelial cell (EC) ETB receptors releases nitric oxide (NO) and prostacyclin (PGI2), which are anti-mitotic and mediate vasodilatation. ETB receptors are also responsible for the clearance of ET-1 from the circulation and renal ETB receptors contribute to sodium and water balance. Pharmacological blockade and genetic models featuring total ETB ablation, demonstrate salt sensitive hypertension. However, these do not allow the role of the EC ETB in cardiovascular homeostasis to be determined. Mice featuring loxP sites flanking exons 3 and 4 of the ETB gene (floxed ETB mice: FF/--) were crossed with Tie2-Cre mice (WW/Tie2-Cre), in which the expression of a Cre recombinase cDNA transgene is limited to EC, to generate EC-specific ETB down-regulated mice (FF/Tie2-Cre). Having demonstrated EC-specific down-regulation of ETB receptors using autoradiography, the role and relative contribution of the EC ETB to the regulation of systemic BP, to the clearance of ET-1 from the plasma, as well as to the development of pulmonary arterial hypertension were investigated. Autoradiography revealed significant down-regulation of ETB in EC-rich tissues such as lung of FF/Tie2-Cre animals (8 ± 3 amol.mm-2) compared to controls (80 ± 21 amol.mm-2) (n=4; p<0.05). Levels of ETA expression were preserved despite higher concentrations of plasma ET-1 in the FF/Tie2-Cre samples (12.4 ± 3.0 pg.ml-1) compared to controls (3.0 ± 0.8 pg.ml-1) (n=6; p<0.001). Using radiotelemetry, mean arterial blood pressure of FF/Tie2 mice was not significantly different to that of FF/- controls on low salt (FF/Tie2-Cre: 122.7 ± 1.52 mmHg, n=10; FF/--: 125.7 ± 0.58 mmHg, n=12), normal salt (FF/Tie2-Cre: 133.8 ± 4.0 mmHg, n=10; FF/--: 131.5 ± 3.33 mmHg, n=12) or high salt diet (FF/Tie2-Cre: 149.2 ± 2.71 mmHg, n=10; FF/--: 143.9 ± 2.97 mmHg, n=12). Similarly no differences in SBP, DBP or HR were seen between genotypes. The clearance of an intravenous bolus of radiolabelled ET-1 was significantly impaired in FF/Tie2-Cre mice (0.054 ± 0.006 ml.sec-1) compared to control mice (0.175 ± 0.032 ml.sec-1) (n=5; p<0.01). ETB blockade of control mice reduced ET-1 clearance to that of untreated FF/Tie2-Cre animals (n=4). Two weeks of hypobaric hypoxia induced an exaggerated increase in systolic right ventricular pressure in FF/Tie2-Cre mice (34.4 ± 1.2 mmHg, n=10) compared with FF/-- mice (24.6 ± 1.4mmHg, n=10; p<0.05), associated with an increased right ventricular/ left ventricular + septum ratio in FF/Tie2-Cre mice (normoxia: 0.224 ± 0.009; hypoxia: 0.285 ± 0.017; p<0.01), but not in FF/-- mice. Hypoxia increased the percentage of remodeled vessels in FF/-- mice (normoxia: 5.6 ± 0.6%; hypoxia: 11.4 ± 0.6%; n=6; p<0.001), and this was augmented in FF/Tie2-Cre mice (normoxia: 7.1 ± 0.5%; hypoxia: 18.5 ± 1.2%; n=6; p<0.001). The EC ETB receptor does not play a significant role in the BP response to salt, suggesting that ETB signalling on other cell types is responsible for ETB mediated natriuresis. However, the EC ETB receptor is crucial to the elimination of ET-1 from the circulation and is protective against the development of pulmonary arterial hypertension, most likely by preventing remodeling of small pulmonary arteries.
2

Van, der Walle Christopher Frederick. "Synthesis and characterisation of an endothelin receptor fragment and an endothelin analogue." Thesis, King's College London (University of London), 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.301137.

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3

Swire, Matthew. "Investigating endothelin receptor B signalling during myelination." Thesis, University of Edinburgh, 2017. http://hdl.handle.net/1842/28912.

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A key process enabling the correct functioning of neural circuits involves the formation of multi‐layered membranous myelin sheaths around axons. Myelin sheaths, made by specialised glial cells called oligodendrocytes in the central nervous system (CNS), metabolically support underlying axons and speed up electrical impulse conduction, aiding efficient communication between neurons. As only a subset of axons in the CNS are myelinated, with unique patterns developed therein, it raises the questions: how does an oligodendrocyte choose which axon to myelinate and what regulates the amount of myelin made? The production of myelin sheaths by the oligodendrocyte, is under strong influence from of a range of signals including those mediated by G protein‐coupled receptor (GPR) superfamily members. One GPR, Endothelin receptor B (EDNRB), best known for regulating blood flow, had previously been demonstrated to both positively and negatively influence myelination. I have investigated how EDNRB regulates myelination using an in vitro myelination assay, alongside in vivo analysis in zebrafish and mice. These systems identified a direct signalling role for EDNRB in the promotion of myelin sheath number. Furthermore, profiling the protein signalling cascade downstream of this receptor identified a range of known and novel factors involved in the regulation of myelin sheath number including the MAPK pathway, Src family kinases, ErbB receptors, protein kinase C ε, NMDAR and AMPAR. Functional analyses of a subset of these factors elucidate how EDNRB signalling, potentially connecting signals from a range of cell types, ensures correct adequate myelination in the CNS.
4

Fukuroda, Takahiro. "STUDIES ON ENDOTHELIN RECEPTOR SUBTYPES MEDIATING ENDOTHELIN ACTION AND CLEARANCE IN THE LUNGS." Kyoto University, 1999. http://hdl.handle.net/2433/182431.

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5

Zhang, Yufeng. "Characteristics of a truncated human endothelin receptor A." Thesis, St George's, University of London, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.300418.

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6

Cid, Graciela Mariana. "Expression and characterization of human endothelin receptor A." Thesis, Birkbeck (University of London), 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.395809.

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7

Bagnall, Alan. "Role of the endothelin B receptor in cardiovascular homeostasis." Thesis, University of Edinburgh, 2004. http://hdl.handle.net/1842/24786.

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The aim of this project was to precisely determine the role of the endothelial cell (EC) ETB receptor in the regulation of vascular tone, blood pressure and clearance of ET-1. Cre-loxP recombination was utilised to conditionally regulate ETB receptor expression in vivo. Mice featuring loxP sites flanking exons 2 and 3 of the ETB receptor gene (floxed ETB receptor mice) were generated by standard gene targeting techniques in embryonic stem cells. Floxed ETB mice were crossed with Tie2-Cre transgenic mice to produce mice in which recombination-mediated removal of ETB receptor coding regions was limited to EC (Flox/Flox Tie2). EC ETB receptor binding of 125I ET-1 and in vitro aortic and tracheal ring myography were performed to assess endothelial function and the response to selective ETB receptor agonists. Pulmonary EC ET-1 binding was decreased by ~80% in EC-specific ETB receptor knockout mice (cpm/50μg membrane protein ± SEM; Flox/Flox Tie2 581 ± 67; W/W -/- 3175 ± 268; n=3; p<0.001). Cell-specificity of ETB receptor down-regulation was demonstrated by maintenance of normal ETB receptor-mediated tracheal constriction. Blood pressure was increased in Flox/Flox Tie2 mice (MAP 137.2 ± 6.4mmHg (n=5); W/W -/-, 113.7 ± 4.7mmHg (n=6; p<0.05) but was not affected by dietary salt. Plasma ET-1 was increased ~4 fold following EC ETB receptor down-regulation (mean plasma [ET-1] pg/ml ± SEM; Flox/Flox Tie2 12.40 ± 2.95; W/W -/- 2.94 ± 0.83; n=6; p<0.001). Aortic rings from Flox/Flox Tie2 mice demonstrated impaired endothelium-dependant vasodilatation to ETB receptor selective agonists and acetylcholine but normal endothelium-independent vasodilatation. Recombination-mediated removal of exons 2 and 3 of the ETB receptor is sufficient to prevent expression of functional ETB receptors. The ‘floxed’ ETB receptor mouse thereby facilitates the cell type-specific down-regulation of ETB receptor expression in vivo. The EC ETB receptor plays an important role in the determination of blood pressure under normal physiological conditions. The mechanism underlying this effect may involve loss of EC ETB receptor-mediated vasodilatation or impaired clearance of ET-1 with a consequent increase in ETA receptor activity.
8

Peter, Markus Guenter. "Endothelin receptor expression in human, rat and porcine heart." Thesis, University of Cambridge, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.627471.

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9

Leslie, Stephen James. "The effect of endothelin A and endothelin B receptor ligands on the cardiovascular system of man." Thesis, University of Edinburgh, 2005. http://hdl.handle.net/1842/29221.

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ET-1 vasoconstricts in the skin microcirculation and it appears that endothelin converting enzyme (ECE) activity is present as big ET-1 also vasoconstricts. ECE and neutral endopeptidase (NEP) blockade both cause vasodilatation suggesting skin basal resting ET tone. ET-1 (1-31) is also a vasoconstrictor in the skin microcirculation. Plasma concentrations of ET-1(1-31) are not elevated in patients with CHF. ETARA improves systemic haemodynamics in patients with CHF while concomitant ETBRA attenuates this effect. In the isolated human myocardium ET is positively inotropic but there is no resting ET inotropy with no effect on basal twitch force with ETRA. In addition, ET attenuates beta-adrenergic activation in isolated human myocardium. In hypercholesterolaemia, forearm vascular effects are similar to those previously reported in healthy volunteers. Treatment with statin therapy for 8 weeks caused a trend towards an increase in ETA mediated vasodilatation. Conclusions: The novel finding that ET(1-31) is a vasoconstrictor in the skin microcirculation may represent a novel pathway of ET production. The haemodynamic benefits of selective ETARA over dual ETA/BRA is a unique finding with considerable importance and supports the development of selective ETARAs as clinical therapies in CHF. The finding of antagonism between the ET system and the beta-adrenergic stimulation may represent a protective adaptation in conditions where there beta-adrenergic stimulation is detrimental and there is activation of the ET system, such as CHF.
10

Elez, Danka. "Production of recombinant human endothelin B receptor in different hosts and its subsequent solubilization and purification." [S.l.] : [s.n.], 2004. http://deposit.ddb.de/cgi-bin/dokserv?idn=970794746.

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Книги з теми "Endothelin receptor":

1

Barton, Matthias. Endothelin in renal physiology and disease. Basel: Karger, 2011.

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2

Mondo, John Paul Di. Isolation and sequencing of the rat endothelin-A receptor (ETA) gene. Ottawa: National Library of Canada, 1996.

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3

Pollock, David M., and Robert F. Highsmith, eds. Endothelin Receptors and Signaling Mechanisms. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-662-11672-2.

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4

NATO, Advanced Study Institute on Vascular Endothelium: Receptors and Transduction Mechanisms (1988 Porto Karras Chalkidikē Greece). Vascular endothelium: Receptors and transduction mechanisms. New York: Plenum Press, 1989.

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5

Boyd, Ryan. Expression and function of endothelin and its receptors in vascular adventitial fibroblasts. St. Catharines, Ont: Brock University, Faculty of Applied Health Sciences, 2007.

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6

Hunt, Jennifer Ann. Characterization of thromboxane receptors on a bovine aortic endothelial cell line. Birmingham: University of Birmingham, 1991.

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7

Inoue, Michitoshi. Regulation of coronary blood flow. London: Springer-Verlag, 1991.

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8

Warner, Timothy D. Endothelin and Its Inhibitors. Springer Berlin / Heidelberg, 2012.

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9

Warner, Timothy D. Endothelin and Its Inhibitors. Springer London, Limited, 2012.

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10

Warner, Timothy D. Endothelin and Its Inhibitors. Springer, 2001.

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Більше джерел

Частини книг з теми "Endothelin receptor":

1

Miyazaki, Hitoshi, Motohiro Kondoh, Yasushi Masuda, Hirotoshi Watanabe, and Kazuo Murakami. "Endothelin Receptors and Receptor Subtypes." In Endothelin, 58–71. New York, NY: Springer New York, 1992. http://dx.doi.org/10.1007/978-1-4614-7514-9_5.

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2

Pollock, David M. "Endothelin Receptor Subtypes and Tissue Distribution." In Endothelin, 1–29. Totowa, NJ: Humana Press, 1998. http://dx.doi.org/10.1007/978-1-4757-2783-8_1.

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3

Warner, Timothy D. "The Development of Specific Endothelin-Receptor Antagonists." In Endothelin, 189–222. Totowa, NJ: Humana Press, 1998. http://dx.doi.org/10.1007/978-1-4757-2783-8_7.

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4

Tasker, Andrew S., and David M. Pollock. "Endothelin Receptors and Receptor Antagonists." In Endothelin Receptors and Signaling Mechanisms, 3–15. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-662-11672-2_2.

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5

Decker, E. Radford, and Tommy A. Brock. "Endothelin Receptor-Signaling Mechanisms in Vascular Smooth Muscle." In Endothelin, 93–119. Totowa, NJ: Humana Press, 1998. http://dx.doi.org/10.1007/978-1-4757-2783-8_4.

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6

Elliott, J. D., and J. N. Xiang. "Endothelin Receptor Antagonists." In Endothelin and Its Inhibitors, 239–70. Berlin, Heidelberg: Springer Berlin Heidelberg, 2001. http://dx.doi.org/10.1007/978-3-642-56899-2_9.

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7

Emoto, Noriaki. "Endothelin Receptor Antagonist." In Diagnosis and Treatment of Pulmonary Hypertension, 153–69. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-287-840-3_12.

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8

Miki, Toru, Randa Hilal-Dandan, Laurence L. Brunton, Jean Sévigny, Kwok-On Lai, Nancy Y. Ip, Renping Zhou, et al. "Endothelin Receptor ETA." In Encyclopedia of Signaling Molecules, 551. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_100390.

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9

Miki, Toru, Randa Hilal-Dandan, Laurence L. Brunton, Jean Sévigny, Kwok-On Lai, Nancy Y. Ip, Renping Zhou, et al. "Endothelin-A Receptor." In Encyclopedia of Signaling Molecules, 551. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_100393.

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10

Clozel, Martine, Alessandro Maresta, and Marc Humbert. "Endothelin Receptor Antagonists." In Handbook of Experimental Pharmacology, 199–227. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-662-45805-1_9.

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Тези доповідей конференцій з теми "Endothelin receptor":

1

Tamkus, D., C. Leece, K. Gallo, BV Madhukar, and N. Dimitrov. "P2-03-06: Endothelin-1/Endothelin A Receptor Signalling in Breast Cancer." In Abstracts: Thirty-Fourth Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 6‐10, 2011; San Antonio, TX. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/0008-5472.sabcs11-p2-03-06.

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2

MacKenzie Ross, Robert V., Mark Southwood, Rhoda Kuc, Guy Hagan, Karen Sheares, David P. Jenkins, Martin Goddard, Anthony P. Davenport, and Joanna Pepke-Zaba. "Endothelin Receptor Distribution In Pulmonary Endarterectomy Tissue." 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.a2413.

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3

Folkert, Ian Wesley, Tsun Ki Jerrick To, Samir Devalaraja, Robert J. Norgard, and Malay Haldar. "Abstract 1776: Tumor-derived endothelins regulate antitumor immune responses through macrophage endothelin B receptor." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-1776.

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4

Ye, Fei, Kazunari Yamada, Yue Liu, Jinny Choe, Anna Dembo, Jonathan L. Tso, Timothy F. Cloughesy, et al. "Abstract 3308: Endothelin 3/endothelin receptor B signaling pathway blockade depletes radio-chemoresistant glioblastoma stem cells." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-3308.

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5

Nagendran, J., G. Sutendra, A. Haromy, DZ Fu, DB Ross, IM Rebeyka, and ED Michelakis. "Endothelin Receptor Inhibitors Decrease Contractility in the Hypertrophied Right Ventricle." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a4141.

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6

Toney, Brent, Amanda Fisher, Marjorie Albrecht, Neel Patel, Robert G. Presson, Jr, Irina Petrache, and Tim Lahm. "Endothelin-A Receptor Blockade Attenuates Pulmonary Vascular Dysfunction Following Experimental Endotoxemia." 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.a6408.

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7

Fox, Benjamin D., David Langleben, Lyda Lesenko, and Andrew Hirsch. "Transition From Sitaxsentan To Other Endothelin Receptor Antagonists - Effects On Hemodynamics." 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.a4798.

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8

Lee, Yao-Ling, and Chuen-Ming Shih. "Association of the endothelin-1 and endothelin A receptor genetic polymorphisms and non-small cell lung cancer in Taiwan." In ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.pa2856.

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9

Vemana, AP, RJ Darrah, RJ Schilz, PG Smith, SD Strausbaugh, and ML Drumm. "High Expression Endothelin Receptor Variants Associate with Lymphangioleiomyomatosis (LAM) and Cystic Fibrosis (CF)." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a4335.

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10

Kosanovic, Djuro, Baktybek Kojonazarov, Bhola K. Dahal, Hossein A. Ghofrani, Norbert Weissmann, Friedrich Grimminger, Werner Seeger, and Ralph T. Schermuly. "A Highly Selective Endothelin-A Receptor Antagonist TBC3711 Reverses Monocrotaline Induced Pulmonary Hypertension." 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.a6316.

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Звіти організацій з теми "Endothelin receptor":

1

Meidan, Rina, and Joy Pate. Roles of Endothelin 1 and Tumor Necrosis Factor-A in Determining Responsiveness of the Bovine Corpus Luteum to Prostaglandin F2a. United States Department of Agriculture, January 2004. http://dx.doi.org/10.32747/2004.7695854.bard.

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Анотація:
The corpus luteum (CL) is a transient endocrine gland that has a vital role in the regulation of the estrous cycle, fertility and the maintenance of pregnancy. In the absence of appropriate support, such as occurs during maternal recognition of pregnancy, the CL will regress. Prostaglandin F2a (PGF) was first suggested as the physiological luteolysin in ruminants several decades ago. Yet, the cellular mechanisms by which PGF causes luteal regression remain poorly defined. In recent years it became evident that the process of luteal regression requires a close cooperation between steroidogenic, endothelial and immune cells, all resident cells of this gland. Changes in the population of these cells within the CL closely consort with the functional changes occurring during various stages of CL life span. The proposal aimed to gain a better understanding of the intra-ovarian regulation of luteolysis and focuses especially on the possible reasons causing the early CL (before day 5) to be refractory to the luteolytic actions of PGF. The specific aims of this proposal were to: determine if the refractoriness of the early CL to PGF is due to its inability to synthesize or respond to endothelin–1 (ET-1), determine the cellular localization of ET, PGF and tumor necrosis factor a (TNF a) receptors in early and mid luteal phases, determine the functional relationships among ET-1 and cytokines, and characterize the effects of PGF and ET-1 on prostaglandin production by luteal cell types. We found that in contrast to the mature CL, administration of PGF2a before day 5 of the bovine cycle failed to elevate ET-1, ETA receptors or to induce luteolysis. In fact, PGF₂ₐ prevented the upregulation of the ET-1 gene by ET-1 or TNFa in cultured luteal cells from day 4 CL. In addition, we reported that ECE-1 expression was elevated during the transitionof the CL from early to mid luteal phase and was accompanied by a significant rise in ET-1 peptide. This coincides with the time point at which the CL gains its responsiveness to PGF2a, suggesting that ability to synthesize ET-1 may be a prerequisite for luteolysis. We have shown that while ET-1 mRNA was exclusively localized to endothelial cells both in young and mature CL, ECE-1 was present in the endothelial cells and steroidogenic cells alike. We also found that the gene for TNF receptor I is only moderately affected by the cytokines tested, but that the gene for TNF receptor II is upregulated by ET-1 and PGF₂ₐ. However, these cytokines both increase expression of MCP-1, although TNFa is even more effective in this regard. In addition, we found that proteins involved in the transport and metabolism of PGF (PGT, PGDH, COX-2) change as the estrous cycle progresses, and could contribute to the refractoriness of young CL. The data obtained in this work illustrate ET-1 synthesis throughout the bovine cycle and provide a better understanding of the mechanisms regulating luteal regression and unravel reasons causing the CL to be refractory to PGF2a.
2

Meidan, Rina, Jorge Flores, Keith Inskeep, and David Wolfenson. Controlling the bovine ovarian cycle by disrupting the endothelin system in corpora lutea and follicles with novel approaches: RNA interference (RNAi) and intra-luteal Atrigel implants. United States Department of Agriculture, June 2006. http://dx.doi.org/10.32747/2006.7695594.bard.

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Анотація:
In summary intensive studies carried out this year in both the US and Israel had established the methodology necessary for the achievement of the specific aims of the original proposal. Two complementary approaches to effectively neutralize the luteal ET- system were developed. In light of recent publications indicating that ET-2 might also have a physiological role in ovulation, the objectives of the original proposal have even more significant. Not only were the technologies to neutralize the luteal endothelin system developed in these studies, but additional important implications about the role of ET-1 were revealed. For example, direct early inhibitory effects of PGF2α were unmasked. It is possible that these early direct inhibitory effects could be related to functional aspects of luteal regression, while the effects observed after 12 hours of the PGF2α injection and that reversed by the ET receptor antagonist, could coincide with structural aspects of regression. Nevertheless, overall, the results clearly indicate that serum progesterone concentrations can effectively be elevated by the receptor antagonist which of great practical importance.
3

Li, Luyuan. Endothelial Cell Specific Receptor TIE-2 as a Therapeutic Target. Fort Belvoir, VA: Defense Technical Information Center, August 1999. http://dx.doi.org/10.21236/ada382384.

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4

Palade, George E. Vascular Endothelial Growth Factor and Receptors in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, April 1999. http://dx.doi.org/10.21236/ada378724.

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5

Quinn, Timothy P. Killing Prostate Cancer Cells and Endothelial Cells with a VEGF-Triggered Cell Death Receptor. Fort Belvoir, VA: Defense Technical Information Center, February 2003. http://dx.doi.org/10.21236/ada415526.

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6

Quinn, Timothy P. Killing Prostate Cancer Cells and Endothelial Cells With a VEGF-Triggered Cell Death Receptor. Fort Belvoir, VA: Defense Technical Information Center, February 2004. http://dx.doi.org/10.21236/ada423810.

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7

Quinn, Timothy P. Killing Prostate Cancer Cells and Endothelial Cells with a VEGF-Triggered Cell Death Receptor. Fort Belvoir, VA: Defense Technical Information Center, June 2005. http://dx.doi.org/10.21236/ada476353.

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8

Thompson, A., C. R. Valeri, and W. Lieberthal. Endothelial Receptor a Blockade Alters the Hemodynamic Response to Nitric Oxide Inhibition in the Rat. Fort Belvoir, VA: Defense Technical Information Center, June 1994. http://dx.doi.org/10.21236/ada360327.

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9

Tan, Linlin, Zhijie Wang, Yuchun Ni, Fupeng Zhang, Zhaowei Huang, Zhipeng Zhang, Jiaqi Yan, and Mei Wu. The efficacy and safety of vascular endothelial growth factor receptor (VEGFR ) inhibitors for recurrent ovarian cancer: a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, February 2021. http://dx.doi.org/10.37766/inplasy2021.2.0019.

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