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Artículos de revistas sobre el tema "Bradykinin B2"

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Publicado: 4 de junio de 2021
Última modificación: 8 de febrero de 2022

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1

Ma, Jie, Yu Luo, Lilin Ge, et al. "Ranakinestatin-PPF from the Skin Secretion of the Fukien Gold-Striped Pond Frog,Pelophylax plancyi fukienensis: A Prototype of a Novel Class of BradykininB2Receptor Antagonist Peptide from Ranid Frogs." Scientific World Journal 2014 (2014): 1–9. http://dx.doi.org/10.1155/2014/564839.

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The defensive skin secretions of many amphibians are a rich source of bradykinins and bradykinin-related peptides (BRPs). Members of this peptide group are also common components of reptile and arthropod venoms due to their multiple biological functions that include induction of pain, effects on many smooth muscle types, and lowering systemic blood pressure. While most BRPs are bradykinin receptor agonists, some have curiously been found to be exquisite antagonists, such as the maximakinin gene-related peptide, kinestatin—a specific bradykinin B2-receptor antagonist from the skin of the giant
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2

Dixon, B. S., R. Breckon, J. Fortune, et al. "Effects of kinins on cultured arterial smooth muscle." American Journal of Physiology-Cell Physiology 258, no. 2 (1990): C299—C308. http://dx.doi.org/10.1152/ajpcell.1990.258.2.c299.

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The present study uses various kinin agonists and antagonists to examine the cellular mechanisms of bradykinin's actions on intracellular calcium, prostaglandins, and adenosine 3',5'-cyclic monophosphate (cAMP) accumulation in cultured arterial smooth muscle cells (casmc) obtained from rat mesenteric arteries. Exposure to bradykinin produced a rapid release of calcium (peak less than or equal to 20 s) from intracellular stores and an increase in prostaglandin (PG) E2 and cAMP production in casmc. Compared with bradykinin, the bradykinin B1-agonist [des-Arg9]BK produced only a small increase in
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3

Willars, Gary B., Werner Müller-Esterl, and Stefan R. Nahorski. "Receptor phosphorylation does not mediate cross talk between muscarinic M3 and bradykinin B2 receptors." American Journal of Physiology-Cell Physiology 277, no. 5 (1999): C859—C869. http://dx.doi.org/10.1152/ajpcell.1999.277.5.c859.

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This study examined cross talk between phospholipase C-coupled muscarinic M3 and bradykinin B2 receptors coexpressed in Chinese hamster ovary (CHO) cells. Agonists of either receptor enhanced phosphoinositide signaling (which rapidly desensitized) and caused protein kinase C (PKC)-independent, homologous receptor phosphorylation. Muscarinic M3 but not bradykinin B2 receptors were also phosphorylated after phorbol ester activation of PKC. Consistent with this, muscarinic M3 receptors were phosphorylated in a PKC-dependent fashion after bradykinin B2 receptor activation, but muscarinic M3 recept
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4

Regoli, D. "Multiple bradykinin B2 receptors." Trends in Pharmacological Sciences 10, no. 4 (1989): 138. http://dx.doi.org/10.1016/0165-6147(89)90163-6.

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5

Pan, H. L., C. L. Stebbins, and J. C. Longhurst. "Bradykinin contributes to the exercise pressor reflex: mechanism of action." Journal of Applied Physiology 75, no. 5 (1993): 2061–68. http://dx.doi.org/10.1152/jappl.1993.75.5.2061.

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This study determined the receptors responsible for mediating bradykinin's effect on skeletal muscle afferents that cause the pressor reflex in anesthetized cats. In eight cats, 1 microgram of bradykinin was injected intra-arterially into the gracilis muscle before and after intravenous injection of a kinin B2-receptor antagonist (NPC 17731, 20 micrograms/kg). Initial injection of bradykinin reflexly increased mean arterial pressure by 23 +/- 7 mmHg, maximal change in pressure over time by 439 +/- 272 mmHg/s, and heart rate by 11 +/- 4 beats/min. The hemodynamic response to bradykinin was abol
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6

Schanstra, Joost P., Johan Duchene, Françoise Praddaude, et al. "Decreased renal NO excretion and reduced glomerular tuft area in mice lacking the bradykinin B2 receptor." American Journal of Physiology-Heart and Circulatory Physiology 284, no. 6 (2003): H1904—H1908. http://dx.doi.org/10.1152/ajpheart.01150.2002.

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Bradykinin B2 receptor knockout mice (B2 −/−) have been useful to study the role of bradykinin under pathological conditions. With the use of these mice, it was shown that bradykinin plays an important role in angiogenesis, heart failure, salt-induced hypertension, and kidney fibrosis. Data on the role of the bradykinin B2 receptor under physiological conditions using these mice are controversial and scarce, because these mice have no typical phenotype. For this reason, we have studied, under physiological conditions, renal hemodynamics as well as a number of morphometric glomerular parameters
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7

Stewart, John M. "Bradykinin B2 receptor antagonists: development and applications." Canadian Journal of Physiology and Pharmacology 73, no. 7 (1995): 787–90. http://dx.doi.org/10.1139/y95-106.

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Most physiological and pathophysiological responses to bradykinin are mediated by G-protein-coupled receptors designated B2 receptors. Discovery of antagonists for these receptors has brought about a revolution in research in the kinin field. The chemistry and development of antagonists for B2 kinin receptors are discussed. Uses of the antagonists in biomedical research and potential clinical applications are presented.Key words: bradykinin antagonists, bradykinin inflammation, bradykinin receptors.
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8

Gröger, Moritz, Diane Lebesgue, Didier Pruneau, et al. "Release of Bradykinin and Expression of Kinin B2 Receptors in the Brain: Role for Cell Death and Brain Edema Formation After Focal Cerebral Ischemia in Mice." Journal of Cerebral Blood Flow & Metabolism 25, no. 8 (2005): 978–89. http://dx.doi.org/10.1038/sj.jcbfm.9600096.

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Pharmacological studies using bradykinin B2 receptor antagonists suggest that bradykinin, an early mediator of inflammation and the main metabolite of the kallikrein-kinin system, is involved in secondary brain damage after cerebral ischemia. However, the time-course of bradykinin production and kinin receptor expression as well as the conclusive role of bradykinin B2 receptors for brain damage after experimental stroke have not been elucidated so far. C57/Bl6 mice were subjected to 45 mins of middle cerebral artery occlusion (MCAO) and 2, 4, 8, 24, and 48 h later brains were removed for the a
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9

Hess, J. Fred, Patricia J. Hey, Tsing-Bau Chen, et al. "Molecular Cloning and Pharmacological Characterization of the Canine B1 and B2 Bradykinin Receptors." Biological Chemistry 382, no. 1 (2001): 123–29. http://dx.doi.org/10.1515/bc.2001.018.

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Abstract The dog is a valuable animal model in the study of the physiological role of both the B1 and B2 bradykinin receptors. To more thoroughly characterize the pharmacological properties of the canine kinin receptors we isolated the cDNA sequence encoding the B1 and B2 bradykinin receptor subtypes and overexpressed them in Chinese hamster ovary (CHO) cells. The cDNA sequence of the canine B1 bradykinin receptor encodes a protein comprised of 350 amino acids that is 76% identical to the human B1 bradykinin receptor. The cDNA sequence of the canine B2 bradykinin receptor encodes a protein of
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10

Xiao, Hong D., Sebastien Fuchs, Justin M. Cole, Kevin M. Disher, Roy L. Sutliff, and Kenneth E. Bernstein. "Role of bradykinin in angiotensin-converting enzyme knockout mice." American Journal of Physiology-Heart and Circulatory Physiology 284, no. 6 (2003): H1969—H1977. http://dx.doi.org/10.1152/ajpheart.00010.2003.

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Angiotensin-converting enzyme (ACE) plays a central role in the renin-angiotensin system. Whereas ACE is responsible for the production of angiotensin II, it is also important in the elimination of bradykinin. Constitutively, the biological function of bradykinin is mediated through the bradykinin B2 receptor. ACE knockout mice have a complicated phenotype including very low blood pressure. To investigate the role of bradykinin in the expression of the ACE knockout phenotype, we bred B2 receptor knockout mice with ACE knockout mice, thus generating a line of mice deficient in both the B2 recep
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11

Brew, E. C., M. B. Mitchell, T. F. Rehring, et al. "Role of bradykinin in cardiac functional protection after global ischemia-reperfusion in rat heart." American Journal of Physiology-Heart and Circulatory Physiology 269, no. 4 (1995): H1370—H1378. http://dx.doi.org/10.1152/ajpheart.1995.269.4.h1370.

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We have reported that cardiac preconditioning against ischemia-reperfusion (IR) can be induced by transient ischemia (TI) and alpha 1-adrenoreceptor stimulation, both mediated by protein kinase C (PKC) (Mitchell, M., X. Meng, C. Parker, E. Brew, A. Harken, and A. Banerjee. Circ. Res. 76: 73-81, 1995). Our study objective was to explore the mechanism of endogenous preconditioning and address the role of PKC activation in bradykinin-mediated cardiac functional protection. Isolated rat heart was used to assess the effects of exogenous bradykinin, TI, selective B2-receptor blocker, and PKC antagon
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12

Gieldon, Artur, Jakob J. Lopez, Clemens Glaubitz, and Harald Schwalbe. "Theoretical Study of the Human Bradykinin-Bradykinin B2 Receptor Complex." ChemBioChem 9, no. 15 (2008): 2487–97. http://dx.doi.org/10.1002/cbic.200800324.

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13

Regoli, Domenico, Nour-Eddine Rhaleb, Stéphane Dion, and Guy Drapeau. "New selective bradykinin receptor antagonists and bradykinin B2 receptor characterization." Trends in Pharmacological Sciences 11, no. 4 (1990): 156–61. http://dx.doi.org/10.1016/0165-6147(90)90067-i.

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14

Ji, Bingyuan, Baohua Cheng, Yanyou Pan, Chunmei Wang, Jing Chen, and Bo Bai. "Neuroprotection of bradykinin/bradykinin B2 receptor system in cerebral ischemia." Biomedicine & Pharmacotherapy 94 (October 2017): 1057–63. http://dx.doi.org/10.1016/j.biopha.2017.08.042.

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15

Nagaki, M., S. Shimura, T. Irokawa, et al. "Bradykinin regulation of airway submucosal gland secretion: role of bradykinin receptor subtype." American Journal of Physiology-Lung Cellular and Molecular Physiology 270, no. 6 (1996): L907—L913. http://dx.doi.org/10.1152/ajplung.1996.270.6.l907.

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To clarify the role of bradykinin receptor subtypes, we examined the effect of bradykinin on feline tracheal and human airway submucosal gland secretion using an isolated gland preparation. Bradykinin induced a significant increase in [3H]glycoconjugate secretion in a dose-dependent manner from isolated glands, which was significantly inhibited by D-Arg-(Hyp3, Thi5,8, D-Phe7)-bradykinin (the B2-receptor antagonist), whereas Des-Arg9-(Leu8)-bradykinin (B1-receptor antagonist) or indomethacin did not significantly alter it. Nitric oxide synthase inhibitor (nitro-L-arginine methyl ester) caused a
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16

Kim, Jenny H., Deepika Jain, Omar Tliba та ін. "TGF-β potentiates airway smooth muscle responsiveness to bradykinin". American Journal of Physiology-Lung Cellular and Molecular Physiology 289, № 4 (2005): L511—L520. http://dx.doi.org/10.1152/ajplung.00027.2005.

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The molecular mechanisms by which bradykinin induces excessive airway obstruction in asthmatics remain unknown. Transforming growth factor (TGF)-β has been involved in regulating airway inflammation and remodeling in asthma, although it is unknown whether TGF-β can modulate bradykinin-associated bronchial hyperresponsiveness. To test whether TGF-β directly modulates airway smooth muscle (ASM) responsiveness to bradykinin, isolated murine tracheal rings were used to assess whether TGF-β alters ASM contractile responsiveness to bradykinin. Interestingly, we found TGF-β-treated murine rings (12.5
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17

Regoli, D., F. Gobeil, Q. T. Nguyen, et al. "Bradykinin receptor types and B2 subtypes." Life Sciences 55, no. 10 (1994): 735–49. http://dx.doi.org/10.1016/0024-3205(94)00557-5.

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18

Takano, Masaoki, and Shogo Matsuyama. "Intracellular and nuclear bradykinin B2 receptors." European Journal of Pharmacology 732 (June 2014): 169–72. http://dx.doi.org/10.1016/j.ejphar.2014.03.011.

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19

Schanstra, Joost, Johan Duchene, Laurence Desmond, et al. "The protective effect of angiotensin converting enzyme inhibition in experimental renal fibrosis in mice is not mediated by bradykinin B2 receptor activation." Thrombosis and Haemostasis 89, no. 04 (2003): 735–40. http://dx.doi.org/10.1055/s-0037-1613580.

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SummaryUnilateral ureteral obstruction (UUO) is an animal model of accelerated renal tubulointerstitial fibrosis. We have recently shown, using this model, that mice lacking the bradykinin B2-receptor (B2-/- ) were more susceptible than control animals to the development of tubulointerstitial fibrosis. Angiotensin converting enzyme (ACE) inhibition slows down UUO-induced renal fibrosis. Since ACE-inhibition increases bradykinin and decreases angiotensin II concentrations we have verified if bradykinin is involved in the antifibrotic effects of ACE-inhibition using the UUO-model and B2-/- mice.
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20

Yau, Lorraine, David P. Wilson, Jeffery P. Werner, and Peter Zahradka. "Bradykinin receptor antagonists attenuate neointimal proliferation postangioplasty." American Journal of Physiology-Heart and Circulatory Physiology 281, no. 4 (2001): H1648—H1656. http://dx.doi.org/10.1152/ajpheart.2001.281.4.h1648.

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Bradykinin has been linked to the development of restenosis in response to vascular injury. We therefore examined the effect of bradykinin on vascular smooth muscle cell growth and neointimal formation in organ culture. Bradykinin stimulated both RNA and DNA synthesis (by 175%) in smooth muscle cells from either porcine or human coronary arteries and increased cell number in a concentration-dependent manner. Both p42/44 mitogen-activated protein kinase (MAPK) and p38 kinase were also activated. Treatment with [Hyp3,Tyr(Me)8]bradykinin, a B2 receptor agonist, stimulated thymidine incorporation
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21

Jong, Y. J., L. R. Dalemar, B. Wilhelm, and N. L. Baenziger. "Human bradykinin B2 receptors isolated by receptor-specific monoclonal antibodies are tyrosine phosphorylated." Proceedings of the National Academy of Sciences 90, no. 23 (1993): 10994–98. http://dx.doi.org/10.1073/pnas.90.23.10994.

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We report the immunoaffinity isolation of bradykinin B2 receptors in a tyrosine-phosphorylated state from WI-38 human lung fibroblasts. We generated six monoclonal antibodies directed against B2 bradykinin receptor biologic activity mediating prostaglandin E2 production in WI-38. These cells express a repertoire of bradykinin receptor affinity forms with closely correlated biologic activity and [3H]bradykinin binding. Some of the monoclonal antibodies selectively recognize intermediate-affinity (Kd = 5.6 nM) or low-affinity (Kd = 42 nM) receptor forms, whereas others recognize epitopes common
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22

Sawutz, David G., Joseph M. Salvino, Ronald E. Dolle, Peter R. Seoane, and Stephen G. Farmer. "Pharmacology and structure – activity relationships of the nonpeptide bradykinin receptor antagonist WIN 64338." Canadian Journal of Physiology and Pharmacology 73, no. 7 (1995): 805–11. http://dx.doi.org/10.1139/y95-109.

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A series of competitive, nonpeptide bradykinin receptor antagonists based on an α-amino acid scaffold have been developed and biologically characterized. The lead compound in the series, WIN 64338, demonstrates competitive inhibition of bradykinin-mediated functional responses through B2 receptors in a variety of tissues and species. WIN 64338 is specific for the bradykinin B2 receptor; it is inactive at both the B1and B3 kinin receptors. In conscious guinea pigs, WIN 64338 inhibits kinin-mediated bronchoconstriction but does not attenuate a similar response to acetylcholine. A series of WIN 6
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23

Blaukat, Andree, Patrick Micke, Irina Kalatskaya, Alexander Faussner, and Werner Müller-Esterl. "Downregulation of bradykinin B2 receptor in human fibroblasts during prolonged agonist exposure." American Journal of Physiology-Heart and Circulatory Physiology 284, no. 6 (2003): H1909—H1916. http://dx.doi.org/10.1152/ajpheart.00034.2003.

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Sustained activation of G protein-coupled receptors results in an attenuation of cellular responses, a phenomenon termed desensitization. Whereas mechanisms for rapid desensitization of ligand-receptor-G protein-effector systems are relatively well characterized, much less is known about long-term adaptation processes that occur in the continuous presence of an agonist. Here we have studied the fate of endogenously expressed bradykinin B2 receptors on human fibroblasts during prolonged agonist treatment. Stimulation with bradykinin for up to 24 h resulted in a 50% reduction of surface binding
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24

HASHII, Minako, Shigeru NAKASHIMA, Shigeru YOKOYAMA, et al. "Bradykinin B2 receptor-induced and inositol tetrakisphosphate-evoked Ca2+ entry is sensitive to a protein tyrosine phosphorylation inhibitor in ras-transformed NIH/3T3 fibroblasts." Biochemical Journal 319, no. 2 (1996): 649–56. http://dx.doi.org/10.1042/bj3190649.

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Signal transduction from mouse bradykinin B2 receptors to calcium influx was studied in ras-transformed NIH/3T3 (DT) fibroblasts. DT cells were preloaded with fura-2 and whole-cell voltage-clamped. Activation of B2 receptors resulted in a decrease of cellular fluorescence at the excitation wavelength of 340, or 360 nm after MnCl2 application, in both the presence and absence of external Ca2+ in DT cells, at a holding potential of -40 mV. This Mn2+ entry through the Ca2+ influx pathway increased with membrane hyperpolarization. Internal application of inositol 1,3,4,5-tetrakisphosphate (InsP4),
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25

Yamawaki, I., P. Geppetti, C. Bertrand, B. Chan, and J. A. Nadel. "Airway vasodilation by bradykinin is mediated via B2 receptors and modulated by peptidase inhibitors." American Journal of Physiology-Lung Cellular and Molecular Physiology 266, no. 2 (1994): L156—L162. http://dx.doi.org/10.1152/ajplung.1994.266.2.l156.

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We studied the effect of exogenous bradykinin on blood flow in the airway microcirculation of anesthetized F344 rats in vivo. We made three successive determinations of airway blood flow and cardiac output using a modification of the reference sample microsphere technique. Injection of bradykinin into the left ventricle increased airway blood flow in a dose-related manner. Pretreatment with the bradykinin B2 receptor antagonist, Hoe 140, completely abolished bradykinin-, but not histamine-induced vasodilation. A bradykinin B1 receptor agonist, [des-Arg9]bradykinin, did not affect airway blood
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26

Zamorano, Rocio, Sunil Suchindran, and James V. Gainer. "3′-Untranslated region of the type 2 bradykinin receptor is a potent regulator of gene expression." American Journal of Physiology-Renal Physiology 290, no. 2 (2006): F456—F464. http://dx.doi.org/10.1152/ajprenal.00009.2005.

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Regulation of the constitutively expressed type 2 bradykinin (B2) receptor, which mediates the principal actions of bradykinin, occurs at multiple levels. The goal of the current study was to determine whether the human B2 3′-untranslated region (UTR) has effects on gene expression, with particular focus on the variable number of tandem repeats (B2-VNTR) polymorphic portion of the 3′-UTR and its flanking AU-rich elements (AREs). When inserted downstream of the luciferase coding region of the pGL3-Promoter vector, the B2-VNTR reduced reporter gene activity by 85% compared with pGL3-Promoter alo
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27

Tsutsui, Masato, Hisashi Onoue, Yasuhiko Iida, Leslie Smith, Timothy O'Brien, and Zvonimir S. Katusic. "B1 and B2 bradykinin receptors on adventitial fibroblasts of cerebral arteries are coupled to recombinant eNOS." American Journal of Physiology-Heart and Circulatory Physiology 278, no. 2 (2000): H367—H372. http://dx.doi.org/10.1152/ajpheart.2000.278.2.h367.

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Our previous ex vivo and in vivo studies reported that expression of the recombinant endothelial nitric oxide (NO) synthase (eNOS) gene in adventitial fibroblasts recovers NO production in arteries without endothelium in response to bradykinin. The present study was designed to characterize subtypes of bradykinin receptors on adventitial fibroblasts coupled to the activation of recombinant eNOS. Endothelium-denuded segments of canine basilar arteries were transduced with β-galactosidase (β-Gal) gene or eNOS gene ex vivo, using a replication-defective adenoviral vector (1010 plaque-forming unit
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28

Haasemann, M., J. Cartaud, W. Muller-Esterl, and I. Dunia. "Agonist-induced redistribution of bradykinin B2 receptor in caveolae." Journal of Cell Science 111, no. 7 (1998): 917–28. http://dx.doi.org/10.1242/jcs.111.7.917.

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Redistribution of receptors within the plasma membrane as well as between the plasma membrane and various cell compartments presents an important way of regulating the cellular responsiveness to their cognate agonists. We have applied immunocytochemical methods to localize the bradykinin B2 receptor and to examine its agonist induced redistribution in A431 cells. In situ labeling with antibodies to ectodomain-2 of the receptor which do not interfere with bradykinin binding of the receptor showed a random distribution of the B2 receptor on the plasma membrane. Stimulation of cells with 20 nM br
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29

Wilkes, B. M., and P. F. Mento. "Bradykinin-induced vasoconstriction and thromboxane release in perfused human placenta." American Journal of Physiology-Endocrinology and Metabolism 254, no. 6 (1988): E681—E686. http://dx.doi.org/10.1152/ajpendo.1988.254.6.e681.

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This investigation was performed to study the effects of bradykinin on the human fetoplacental circulation. The artery to a single placental cotyledon was perfused with RPMI medium (0.764 ml/min). Bradykinin caused a dose-related increase in vascular resistance. Because bradykinin is generally a vasodilator, we investigated the possibility that bradykinin-induced vasoconstriction was due to interactions with other pressor systems. Bradykinin and 9,11-dideoxy-9 alpha, 11 alpha-epoxymethanoprostaglandin F2 alpha (a stable thromboxane agonist) caused a dose-related increase in perfusion pressure.
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30

Rhaleb, Nour-Eddine, Noureddine Rouissi, Guy Drapeau, Daniela Jukic, and Domenico Regoli. "Characterization of bradykinin receptors in peripheral organs." Canadian Journal of Physiology and Pharmacology 69, no. 7 (1991): 938–43. http://dx.doi.org/10.1139/y91-142.

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Bradykinin (BK) and related kinins are potent stimulants of the rabbit jugular vein, the hamster urinary bladder, and the guinea pig trachea. The characterization of kinin receptors in these tissues was made with agonists and antagonists. Results obtained with agonists indicate that bradykinin and kallidin are much more active than des-Arg9-BK and suggest the presence of B2 receptors in the three organs. Some new agonists were also tested and the BK analogue, [Hyp3,Tyr(Me)8]BK, was found to be a potent and selective stimulant of the three preparations, with pD2 values of 8.56, 8.00, and 8.39,
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31

Park, Tae-Ju, and Kyong-Tai Kim. "Activation of B2 bradykinin receptors by neurotensin." Cellular Signalling 15, no. 5 (2003): 519–27. http://dx.doi.org/10.1016/s0898-6568(02)00136-5.

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32

Buchinger, Peter, and Joachim Rehbock. "The Bradykinin B2-Receptor in Human Decidua." Seminars in Thrombosis and Hemostasis 25, no. 06 (1999): 543–49. http://dx.doi.org/10.1055/s-2007-994963.

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33

Chen, Er-Yun, Dwaine F. Emerich, Raymond T. Bartus, and Jeffrey H. Kordower. "B2 bradykinin receptor immunoreactivity in rat brain." Journal of Comparative Neurology 427, no. 1 (2000): 1–18. http://dx.doi.org/10.1002/1096-9861(20001106)427:1<1::aid-cne1>3.0.co;2-0.

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34

Regoli, D., N. E. Rhaleb, C. Tousignant, et al. "New highly potent bradykinin B2 receptor antagonists." Agents and Actions 34, no. 1-2 (1991): 138–41. http://dx.doi.org/10.1007/bf01993260.

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35

Lehmberg, Jens, Jürgen Beck, Alexander Baethmann, and Eberhard Uhl. "Bradykinin Antagonists Reduce Leukocyte–Endothelium Interactions after Global Cerebral Ischemia." Journal of Cerebral Blood Flow & Metabolism 23, no. 4 (2003): 441–48. http://dx.doi.org/10.1097/01.wcb.0000052280.23292.35.

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The aim of the present study was to evaluate the influence of bradykinin on microcirculatory changes and outcome after global cerebral ischemia (15 minute) in Mongolian gerbils. The cerebral microcirculation was investigated by fluorescent intravital microscopy. Survival and functional outcome was evaluated up to 4 d after ischemia. Animals were treated with the selective B1 and B2 receptor antagonists B 9858 and CP 0597, respectively, and the nonselective B1/B2 receptor antagonist B 9430. Leukocyte activation was significantly reduced by all antagonists as indicated by a significant decrease
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36

Morgan-Boyd, R., J. M. Stewart, R. J. Vavrek, and A. Hassid. "Effects of bradykinin and angiotensin II on intracellular Ca2+ dynamics in endothelial cells." American Journal of Physiology-Cell Physiology 253, no. 4 (1987): C588—C598. http://dx.doi.org/10.1152/ajpcell.1987.253.4.c588.

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The purpose of this study was to investigate the effects of angiotensin II and bradykinin on intracellular Ca2+ dynamics in cultured endothelial cells. We used the "second-generation" fluorescent Ca2+ indicator fura-2, in conjunction with dual-wavelength fluorescence spectroscopy, in cultured adherent pulmonary arterial endothelial cells. Angiotensin II (up to 2 microM) had no consistent effect on intracellular Ca2+ levels. In contrast, bradykinin (10 nM) elicited a transient increase of cytosolic free Ca2+, from the resting value of 37 +/- 5 to 647 +/- 123 nM, followed by a decline to a stead
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37

Figueroa, C. D., C. B. Gonzalez, S. Grigoriev, et al. "Probing for the bradykinin B2 receptor in rat kidney by anti-peptide and anti-ligand antibodies." Journal of Histochemistry & Cytochemistry 43, no. 2 (1995): 137–48. http://dx.doi.org/10.1177/43.2.7822771.

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The kallikrein-kinin system is involved in the inflammatory process, in blood pressure regulation, and in renal homeostasis. The presence of kallikreins, kininogens, and kinins in renal tissues and fluids is well established; however, the occurrence and distribution of the bradykinin (B2) receptor in the kidney are unknown. Using chemically cross-linked conjugates of bovine serum albumin and the B2 agonist bradykinin or the potent B2 antagonist HOE140, followed by antibodies to the respective ligand and the peroxidase-anti-peroxidase system, we were able to detect the B2 receptor. The receptor
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38

Lavoie, Julie L., and Louise Béliveau. "Bradykinin facilitates noradrenaline spillover during contraction in the canine gracilis muscle." Canadian Journal of Physiology and Pharmacology 79, no. 10 (2001): 831–35. http://dx.doi.org/10.1139/y01-062.

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Noradrenaline spillover from skeletal muscle vascular areas increases during exercise but the underlying mechanisms are not well understood. Muscle contraction itself causes changes in many factors that could affect noradrenaline spillover. For instance, it has been reported that bradykinin is synthesized in skeletal muscle areas during contraction. Because the B2 bradykinin receptor facilitates noradrenaline spillover, it may be involved in the increase associated with contraction. In this experiment, we studied the effect of bradykinin on noradrenaline spillover in the in situ canine gracili
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39

Trabold, Raimund, Christian Erös, Klaus Zweckberger, et al. "The Role of Bradykinin B1 and B2 Receptors for Secondary Brain Damage after Traumatic Brain Injury in Mice." Journal of Cerebral Blood Flow & Metabolism 30, no. 1 (2009): 130–39. http://dx.doi.org/10.1038/jcbfm.2009.196.

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Inflammatory mechanisms are known to contribute to the pathophysiology of traumatic brain injury (TBI). Since bradykinin is one of the first mediators activated during inflammation, we investigated the role of bradykinin and its receptors in posttraumatic secondary brain damage. We subjected wild-type (WT), B1-, and B2-receptor-knockout mice to controlled cortical impact (CCI) and analyzed tissue bradykinin as well as kinin receptor mRNA and protein expression up to 48 h thereafter. Brain edema, contusion volume, and functional outcome were assessed 24 h and 7 days after CCI. Tissue bradykinin
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40

Gauthier, Kathryn M., Cody J. Cepura, and William B. Campbell. "ACE inhibition enhances bradykinin relaxations through nitric oxide and B1 receptor activation in bovine coronary arteries." Biological Chemistry 394, no. 9 (2013): 1205–12. http://dx.doi.org/10.1515/hsz-2012-0348.

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Abstract Bradykinin causes vascular relaxations through release of endothelial relaxing factors including prostacyclin, nitric oxide (NO) and epoxyeicosatrienoic acids (EETs). Bradykinin is metabolized by angiotensin converting enzyme (ACE) and ACE inhibition enhances bradykinin relaxations. Our goal was to characterize the role of bradykinin receptors and endothelial factors in ACE inhibitor-enhanced relaxations in bovine coronary arteries. In U46619 preconstricted arteries, bradykinin (10-11-10-8m) caused concentration-dependent relaxations (maximal relaxation ≥100%, log EC50=-9.8±0.1). In t
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41

Maruo, Keishi, Takaaki Akaike, Tomomichi Ono, and Hiroshi Maeda. "Involvement of Bradykinin Generation in Intravascular Dissemination of Vibrio vulnificus and Prevention of Invasion by a Bradykinin Antagonist." Infection and Immunity 66, no. 2 (1998): 866–69. http://dx.doi.org/10.1128/iai.66.2.866-869.1998.

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ABSTRACT Involvement of bradykinin generation in bacterial invasion was examined by using a gram-negative bacillus, Vibrio vulnificus, which is known to invade the blood circulatory system and cause septicemia. V. vulnificus was injected intraperitoneally (i.p.) into mice with or without bradykinin or a bradykinin (B2 receptor) antagonist. Dissemination of V. vulnificus from peritoneal septic foci to the circulating blood was assessed by counting of viable bacteria in venous blood by use of the colony-forming assay. Intravascular dissemination of V. vulnificus in mice was significantly potenti
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42

Singh, Padmasana, Amitabh Krishna, and Rajagopala Sridaran. "Changes in bradykinin and bradykinin B2-receptor during estrous cycle of mouse." Acta Histochemica 113, no. 4 (2011): 436–41. http://dx.doi.org/10.1016/j.acthis.2010.03.008.

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43

Borkowski, Joseph A., and J. Fred Hess. "Targeted disruption of the mouse B2 bradykinin receptor in embryonic stem cells." Canadian Journal of Physiology and Pharmacology 73, no. 7 (1995): 773–79. http://dx.doi.org/10.1139/y95-104.

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Two mammalian genes encoding bradykinin (BK) receptors termed B1 and B2 have been identified by molecular cloning techniques. Some pharmacological data suggest the existence of further subtypes of the B2 receptor. To unambiguously determine whether additional genes encoding B2 BK receptors might exist in mammals, steps have been taken toward the generation of mice with a "knockout" of the BK B2 receptor. A genomic clone of the mouse B2 BK receptor was isolated and its coding sequence determined by DNA sequence analysis. A physical map of the DNA flanking this coding sequence was generated. A v
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44

Yogi, Alvaro, Glaucia E. Callera, Rita Tostes, and Rhian M. Touyz. "Bradykinin regulates calpain and proinflammatory signaling through TRPM7-sensitive pathways in vascular smooth muscle cells." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 296, no. 2 (2009): R201—R207. http://dx.doi.org/10.1152/ajpregu.90602.2008.

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Transient receptor potential melastatin-7 (TRPM7) channels have recently been identified to be regulated by vasoactive agents acting through G protein-coupled receptors in vascular smooth muscle cells (VSMC). However, downstream targets and functional responses remain unclear. We investigated the subcellular localization of TRPM7 in VSMCs and questioned the role of TRPM7 in proinflammatory signaling by bradykinin. VSMCs from Wistar-Kyoto rats were studied. Cell fractionation by sucrose gradient and differential centrifugation demonstrated that in bradykinin-stimulated cells, TRPM7 localized in
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45

Mio, Tadashi, Xiangde Liu, Myron L. Toews, et al. "Bradykinin augments fibroblast-mediated contraction of released collagen gels." American Journal of Physiology-Lung Cellular and Molecular Physiology 281, no. 1 (2001): L164—L171. http://dx.doi.org/10.1152/ajplung.2001.281.1.l164.

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Bradykinin is a multifunctional mediator of inflammation believed to have a role in asthma, a disorder associated with remodeling of extracellular connective tissue. Using contraction of collagen gels as an in vitro model of wound contraction, we assessed the effects of bradykinin tissue on remodeling. Human fetal lung fibroblasts were embedded in type I collagen gels and cultured for 5 days. After release, the floating gels were cultured in the presence of bradykinin. Bradykinin significantly stimulated contraction in a concentration- and time-dependent manner. Coincubation with phosphoramido
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46

Santiago, J. A., E. A. Garrison, and P. J. Kadowitz. "Analysis of responses to bradykinin: effects of Hoe-140 in the hindquarters vascular bed of the cat." American Journal of Physiology-Heart and Circulatory Physiology 267, no. 2 (1994): H828—H836. http://dx.doi.org/10.1152/ajpheart.1994.267.2.h828.

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The mechanisms and receptor subtype mediating vasodilator responses to bradykinin were investigated in the hindquarters vascular bed of the cat under constant flow conditions. Intraarterial injections of bradykinin in doses of 10–1,000 ng into the hindquarters vascular bed caused dose-related decreases in perfusion pressure that were inhibited by Hoe-140, a bradykinin B2-receptor antagonist. Injections of des-Arg9-bradykinin (in doses 10-fold higher than for bradykinin) caused smaller dose-related decreases in hindquarters perfusion pressure that were not blocked by Hoe-140. Administration of
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47

Feletou, M., M. Germain, and B. Teisseire. "Converting-enzyme inhibitors potentiate bradykinin-induced relaxation in vitro." American Journal of Physiology-Heart and Circulatory Physiology 262, no. 3 (1992): H839—H845. http://dx.doi.org/10.1152/ajpheart.1992.262.3.h839.

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Experiments were designed to study the effects of converting-enzyme inhibitors (captopril and S 10211) on the endothelium-dependent relaxation to bradykinin in isolated porcine arteries. Rings of femoral arteries with and without endothelium were suspended in organ chambers to record isometric tension. Rings of coronary arteries without endothelium were used as bioassay tissue to record release of endothelium-derived relaxing factor (EDRF) from perfused femoral arteries. In organ chambers, bradykinin induced endothelium-dependent relaxation and, inconsistently, endothelium-independent contract
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48

Kugaevskaya, E. V., and Yu E. Elisseeva. "Ace inhibitors - activators of kinin receptors." Biomeditsinskaya Khimiya 57, no. 3 (2011): 282–99. http://dx.doi.org/10.18097/pbmc20115703282.

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Angiotensin converting enzyme (ACE) inhibitors are widely used for treatment of cardiovascular diseases. The effects of ACE inhibitors on the human bradykinin receptors were investigated. The mode of action of ACE inhibitors is considered. There is evidence that ACE inhibitors exert effects on the vascular system that cannot be attributed simply to the inhibition of ACE activity and accumulation of locally produced bradykinin. ACE inhibitors augment bradykinin effects on receptors indirectly by inducing cross-talk between ACE and the B2 receptor when enzyme and receptor molecules are stericall
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49

Asano, Masayuki, Hiroe Sawai, Chie Hatori, Noriaki Inamura, Tatsujiro Fujiwara, and Kunio Nakahara. "Effects of a nonpeptide bradykinin B2 receptor antagonist, FR167344, on guinea-pig tracheal smooth muscle bradykinin receptors." Canadian Journal of Physiology and Pharmacology 76, no. 10-11 (1998): 1051–55. http://dx.doi.org/10.1139/y98-098.

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It is speculated that bradykinin may play an important role in asthma. Thus, bradykinin receptor antagonists may have therapeutic potential against asthma. Orally active bradykinin antagonists would be more desirable for the treatment of the disease. In the present study, we examined the effects of a novel, potent, selective, and orally active nonpeptide bradykinin B2 receptor antagonist, FR167344 (N-[N-[3-[(3-bromo-2-methylimidazo[1,2-a]pyridin-8-yl)oxymethyl]- 2,4-dichlorophenyl]-N-methylaminocarbonylmethyl]-4-(dimethylaminocarbonyl)cinnamylamide hydrochloride), on guinea-pig tracheal smooth
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50

Shigematsu, Sakuji, Shuji Ishida, Dean C. Gute, and Ronald J. Korthuis. "Bradykinin-induced proinflammatory signaling mechanisms." American Journal of Physiology-Heart and Circulatory Physiology 283, no. 6 (2002): H2676—H2686. http://dx.doi.org/10.1152/ajpheart.00538.2002.

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Intravital microscopic techniques were used to examine the mechanisms underlying bradykinin-induced leukocyte/endothelial cell adhesive interactions (LECA) and venular protein leakage (VPL) in single postcapillary venules of the rat mesentery. The effects of bradykinin superfusion to increase LECA and VPL were prevented by coincident topical application of either a bradykinin-B2 receptor antagonist, a cell-permeant superoxide dismutase (SOD) mimetic or antioxidant, or inhibitors of cytochrome P-450 epoxygenase (CYPE) or protein kinase C (PKC) but not by concomitant treatment with either SOD, a
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