Relevant bibliographies by topics / Bradykinin

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Academic literature on the topic 'Bradykinin'

Author: Grafiati
Published: 4 June 2021
Last updated: 9 March 2023

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Journal articles on the topic "Bradykinin"

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Dixon, B. S., R. Breckon, J. Fortune, R. J. Vavrek, J. M. Stewart, R. Marzec-Calvert, and S. L. Linas. "Effects of kinins on cultured arterial smooth muscle." American Journal of Physiology-Cell Physiology 258, no. 2 (February 1, 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 intracellular calcium. The bradykinin-mediated increase in intracellular calcium was competitively blocked by the B2 receptor antagonist [D-Arg-O-Hyp3-Thi5,8-D-Phe7]BK (B4307) but not the B1-antagonist ([des-Arg9-Leu8]BK). In addition, the similarity of the dose-response curves for the bradykinin-mediated increase in Ca2+, PGE2, and cAMP (half-maximal stimulation of 12, 11, and 13 nM, respectively) and the ability of the B2-antagonist (B4307) to block each of these effects of bradykinin suggest that all three effects are mediated by the same bradykinin (B2) receptor. Further studies revealed that increases in intracellular calcium are necessary for the bradykinin-mediated increase in PGE2 formation and the subsequent PGE2-dependent formation of cAMP. Taken together, these results suggest that bradykinin acts via a B2-receptor on arterial smooth muscle cells to release calcium from intracellular stores, leading to increases in PGE2 production and the PGE2-dependent activation of adenylate cyclase.
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Ma, Jie, Yu Luo, Lilin Ge, Lei Wang, Mei Zhou, Yingqi Zhang, Jinao Duan, Tianbao Chen, and Chris Shaw. "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 fire-bellied toad,Bombina maxima. Here, we describe the identification, structural and functional characterization of a heptadecapeptide (DYTIRTRLHQGLSRKIV), named ranakinestatin-PPF, from the skin of the Chinese ranid frog,Pelophylax plancyi fukienensis, representing a prototype of a novel class of bradykinin B2-receptor specific antagonist. Using a preconstricted preparation of rat tail arterial smooth muscle, a single dose of 10−6 M of the peptide effectively inhibited the dose-dependent relaxation effect of bradykinin between 10−11 M and 10−5 M and subsequently, this effect was pharmacologically-characterized using specific bradykinin B1- (desArg-HOE140) and B2-receptor (HOE140) antagonists; the data from which demonstrated that the antagonism of the novel peptide was mediated through B2-receptors. Ranakinestatin—PPF—thus represents a prototype of an amphibian skin peptide family that functions as a bradykinin B2-receptor antagonist herein demonstrated using mammalian vascular smooth muscle.
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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 (November 1, 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 receptor activation did not influence bradykinin B2receptor phosphorylation. Despite heterologous phosphorylation of muscarinic M3 receptors, phosphoinositide and Ca2+signaling were unaffected. In contrast, marked heterologous desensitization of bradykinin-mediated responses occurred despite no receptor phosphorylation. This desensitization was associated with a sustained component of muscarinic receptor-mediated signaling, whereas bradykinin's inability to influence muscarinic receptor-mediated responses was associated with rapid and full desensitization of bradykinin responses. Thus the mechanism of functional cross talk most likely involves depletion of a shared signaling component. These data demonstrate that receptor phosphorylation is not a prerequisite for heterologous desensitization and that such desensitization is not obligatory after heterologous receptor phosphorylation.
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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 (October 1, 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 steady-state value of 113 +/- 14 nM, which was significantly higher than the resting Ca2+ levels. Bradykinin's Ca-stimulatory effect was dose dependent, having a half-maximally effective concentration of approximately 1 nM and a maximally effective concentration of 10 nM. A B1-receptor agonist, Des-Arg9-bradykinin, was much less effective than bradykinin as modulator of cytosolic Ca2+. Moreover, a B1-receptor antagonist, Des-Arg9, [Leu8]-bradykinin, did not significantly affect the increase of cytosolic Ca2+ elicited by bradykinin. On the other hand, the bradykinin-elicited increase of Ca2+ was almost completely inhibited by a novel B2-receptor antagonist, D-Arg-[Hyp3, Thi5,8, D-Phe7]-bradykinin. Bradykinin increased cytosolic free Ca2+ levels in cells maintained in Ca2+-deficient extracellular medium, suggesting that the peptide mobilized Ca2+ from intracellular stores. However, the absence of extra-cellular Ca2+ resulted in an 80-90% attenuation of the transient Ca2+ response, whereas the posttransient steady-state response was completely absent. These findings are consistent with the notion that the bradykinin-elicited transient Ca2+ response is dependent on both extra- and intracellular Ca2+ and that the posttransient steady-state response is entirely dependent on extracellular Ca2+. Endothelial cells were responsive to a second dose of bradykinin after a 10-min interim period of incubation in the absence of the peptide hormone. The absence of extracellular Ca2+ during the interim period, or the pretreatment of cells with ionomycin in the absence of extracellular Ca2+, prevented the response of the cells to a second dose of bradykinin. Bradykinin- or ionomycin-desensitized cells could be resensitized by a brief incubation period in Ca2+-replete medium. The results are consistent with the notions that cellular resensitization requires the replenishment of intracellular Ca2+ and that bradykinin, but not angiotensin II, modulates intracellular Ca2+ dynamics in endothelial cells by interacting with a B2-type receptor.
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CUGNO, Massimo, Francesco SALERNO, Jürg NUSSBERGER, Bianca BOTTASSO, Elettra LORENZANO, and Angelo AGOSTONI. "Bradykinin in the ascitic fluid of patients with liver cirrhosis." Clinical Science 101, no. 6 (November 20, 2001): 651–57. http://dx.doi.org/10.1042/cs1010651.

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Bradykinin, a nonapeptide with vasodilatory and permeabilizing activity, is generated through the cleavage of high-Mr (‘high-molecular-weight’) kininogen by kallikrein, and its generation is facilitated by plasmin. In the ascitic fluid of patients with cirrhosis, there is massive cleavage of high-Mr kininogen and activation of fibrinolysis, but bradykinin has never been measured directly. In the ascitic fluid of 24 patients with cirrhosis, we measured bradykinin-(1-9)-nonapeptide levels by RIA after liquid-phase and subsequent HPLC extraction, and those of its catabolic product bradykininin-(1-5)-pentapeptide by ELISA after liquid-phase extraction. Cleaved high-Mr kininogen, activated factor XII and plasmin-antiplasmin complexes were measured in ascitic fluid and plasma. Plasma renin activity (PRA) was also determined. As a control, we also analysed plasma from 24 healthy subjects matched for sex and age with the patients. In the ascitic fluid from patients with cirrhosis, the median bradykinin-(1-9) concentration was 3.3fmol/ml (range 0.2-29.0fmol/ml), and the median bradykinin-(1-5) concentration was 210fmol/ml (range 58-7825 fmol/ml). The levels of bradykinin-(1-5) in ascitic fluid were higher in patients with refractory ascites [median 1091fmol/ml (range 58-7825fmol/ml)] than in patients with responsive ascites [134 fmol/ml (72-1084fmol/ml)] (P = 0.010). Ascitic fluid levels of bradykinin-(1-9) were not related to the severity of ascites. PRA was higher in patients with refractory ascites [23.0ngċh-1ċml-1 (7.9-80.0ngċh-1ċml-1)] than in patients with responsive ascites [6.9ngċh-1ċml-1 (0.9-29.4ngċh-1ċml-1)] (P = 0.002). In ascitic fluid, 48% (19-68%) of high-Mr kininogen was cleaved, and plasmin-antiplasmin complexes were more concentrated than in plasma (P = 0.0001). In conclusion, in the ascitic fluid of patients with cirrhosis, both bradykinin-(1-9) and bradykinin-(1-5) are present, with cleavage of high-Mr kininogen and activation of fibrinolysis. The highest levels of the long-lived metabolite bradykinin-(1-5) were found in the ascitic fluid of patients with refractory ascites and high PRA. Activation of the kinin system may therefore be involved in decompensating cirrhosis, but a cause-effect relationship remains to be established.
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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 (November 1, 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 abolished by kinin B2-receptor blockade. Similar injection of the kinin B1-receptor agonist des-Arg9-bradykinin caused no cardiovascular responses (n = 6). In eight different animals, mean arterial pressure, maximal change in left ventricular pressure over time, and heart rate responses to 30 s of electrically stimulated hindlimb contraction were attenuated by 50 +/- 6, 55 +/- 7, and 41 +/- 8%, respectively, after kinin B2-receptor blockade. In eight other animals, mean arterial pressure, maximal change in left ventricular pressure over time, and heart rate responses were reduced by 58 +/- 8, 66 +/- 6, and 40 +/- 12%, respectively, after inhibition of prostaglandin synthesis with indomethacin (2.5–3 mg/kg iv) and were then abolished by subsequent B2-receptor blockade. These data suggest that bradykinin contributes to the exercise pressor reflex through its action on kinin B2 receptors located on the nerve endings of the muscle afferents.(ABSTRACT TRUNCATED AT 250 WORDS)
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Todoriko, L. D. "Problem issues of the pathogenesis of inflammatory reaction and the course of coronavirus infection." Tuberculosis, Lung Diseases, HIV Infection, no. 1 (March 23, 2021): 76–86. http://dx.doi.org/10.30978/tb2021-1-76.

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Objective — to analysis and systematization of literature data about pathogenesis of the inflammatory reaction and the clinical course of coronavirus infection caused by SARS-CoV-2. Materials and methods. Access to various full-text and abstract databases was used for the search query «coronavirus», «COVID-19», «SARS-CoV-2» and their systematic evaluation was carried out. The most complete database of available literature sources (about 70) was obtainedon the molecular pathophysiology of COVID-19. Results and discussion. The results of the analysis of the molecular pathophysiology of COVID-19 showed that the biomedical terms associated with COVID-19/SARS-CoV-2 form several clusters: cluster 1 is inflammation and the formation of a cytokine storm; cluster 2 — pathophysiological justification of the treatment of coronavirus infection, cluster 3 — comorbid conditions. Analytics of cluster 1 showed one of the most interesting working hypotheses today is model of bradykinin storm. This hypothesis can explain the multisymptomatic nature of COVID-19, including some of its strangest manifestations. The essence of the theory of bradykinin is that, when the virus begins to affect the regulation of renin-angiotensin-aldosterone system (RAAS) through the activation of angio­tensin-converting enzyme type II, it causes the mechanisms that regulate bradykinin levels to fail. Bradykinin’s receptors repeatedly are sensitized and the body also ceases to efficiently break down bradykinin. ACE break down bradykinin, but when the virus suppresses its activity, it cannot work with the same efficiency. The end result of such an imbalance is the release of excessive amounts of bradykinin, due to its mass unrestrained accumulation with the formation of a phenomenon — bradykinin storm. According to the bradykinin hypothesis, this particular variant of the storm is ultimately responsible for the polymorbidity of the clinical picture and the fatal effects cause d by COVID-19. Conclusions. The bradykinin hypothesis of the development of a systemic inflammatory response in SARS-CoV-2 virus is a model that contributes to a better understanding of the pathogenesis and course of COVID-19 and adds novelty to data that are already known. It predicts almost all known symptoms today and offers quality treatments for the disease. Analysis of the processed data from the literature of cluster 2, devoted to the pathophysiological rationale treatment of coronavirus infection led to the role of vitamin D — as a nutrient involved in regulatory processes with participation of RAAS.
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Sheikh, Iftikhar A., and Allen P. Kaplan. "Studies of the digestion of bradykin, lys-bradykinin, and des-Arg9-bradykinin by angiotensin converting enzyme." Biochemical Pharmacology 35, no. 12 (June 1986): 1951–56. http://dx.doi.org/10.1016/0006-2952(86)90726-4.

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Gouda, Ahmed S., and Bruno Mégarbane. "Molecular Bases of Serotonin Reuptake Inhibitor Antidepressant-Attributed Effects in COVID-19: A New Insight on the Role of Bradykinins." Journal of Personalized Medicine 12, no. 9 (September 11, 2022): 1487. http://dx.doi.org/10.3390/jpm12091487.

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Widely available effective drugs to treat coronavirus disease-2019 (COVID-19) are still limited. Various studies suggested the potential contribution of selective serotonin-reuptake inhibitor (SSRI) antidepressants to alleviate the clinical course of COVID-19. Initially, SSRI antidepressant-attributed anti-COVID-19 activity was attributed to their direct agonistic or indirect serotonin-mediated stimulation of sigma-1 receptors (Sig1-R). Thereafter, attention was drawn to the property of SSRI antidepressants to decrease ceramide production, as functional inhibitors of acid sphingomyelinase. Ceramides are cell membrane waxy lipids formed by sphingosine and a fatty acid, playing a major role in receptor signaling and infection. In COVID-19 patients, ceramide production is increased due to acid sphingomyelinase activation. Here, we aimed to review the relationships between bradykinins and the proposed pathways supporting SSRI antidepressant-attributed effectiveness in COVID-19. In COVID-19 patients, bradykinin receptor-B1 stimulation is enhanced following the downregulation of angiotensin-converting enzyme-2, which is responsible for the inactivation of des-Arg9-bradykinin, a bradykinin metabolite, contrasting with the decrease in bradykinin receptor-B2 (BDKRB2) stimulation, which results from the inhibition of cathepsin L, a kininogenase involved in bradykinin production and present at the infection site. Sig1-R stimulation modulates the inflammatory response by regulating cytokine production and counterbalances COVID-19-attributed BDKRB2 inhibition by potentiating its effects on the cytosolic calcium concentration. Moreover, the beneficial effects obtained with acid sphingomyelinase inhibition are parallel to those expected with BDKRB2 stimulation in COVID-19. Altogether, these findings suggest that one ultimate pathway of SSRI antidepressant-attributed anti-COVID-19 activity is the potentiation of BDKRB2 effects shown to be inhibited in COVID-19. In conclusion, SSRI antidepressants are able to interact positively with the pathophysiological mechanisms involved in COVID-19. However, their exact benefits in preventing morbidities or improving the outcome in COVID-19 patients remain unknown.
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Öztürk, Yusuf, V. Melih Altan, Nuray Yıdızoğlu-Arı, and Orhan Altınkurt. "Bradykinin receptors in intestinal smooth muscles and their post-receptor events related to calcium." Mediators of Inflammation 2, no. 4 (1993): 309–15. http://dx.doi.org/10.1155/s0962935193000432.

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The effects of trifluoperazine and verapamil on bradykinin- and des-Arg9-bradykinin induced responses of isolated rat duodenum and guinea-pig ileum were investigated to elucidate post-bradykinin receptor events. Verapamil and trifluoperazine inhibited bradykinin induced relaxations and contractions and des-Arg9- bradykinin induced contractions in rat duodenum. Bradykinin induced contractions of ileum were also inhibited by trifluoperazine and. verapamil. Since non-competitive affinity constants of trifluoperazine and verapamil for the relaxant responses to bradykinin in duodenum and for the contractile responses to bradykinin in ileum are different, post-bradykinin receptor events related to calcium may be different in ileum and duodenum. In addition, affinity constants of bradykinin in guinea-pig ileum and rat duodenum are also disparate suggesting the presence of different types of bradykinin B2receptors in these two organs.
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Dissertations / Theses on the topic "Bradykinin"

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UENO, Tomoyuki, Yasuko KOZAKI, and Kazue MIZUMURA. "Increased Expression of mRNA for B1 and B2 Bradykinin Receptors in the Skin of Adjuvant Inoculated Rats." Research Institute of Environmental Medicine, Nagoya University, 2002. http://hdl.handle.net/2237/2787.

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Willer, Elizabeth Jane. "Control of B2 bradykinin receptor gene expression." Thesis, University College London (University of London), 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.286487.

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Owen, Penelope Jane. "Bradykinin stimulation of bovine adrenal chromaffin cells." Thesis, University of Leicester, 1991. http://hdl.handle.net/2381/33600.

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Cultured bovine adrenal chromaffin cells provide a useful model of stimulus secretion coupling and respond to cholinergic agonists by secreting catecholamines. Work in this thesis concentrates on the responses to a non-cholinergic agonist, bradykinin. Bradykinin as shown to stimulate a two phase, dose dependent increase in catecholamine release which is mediated by a receptor of the B2 subtype. Calcium entry is shown to be required for release to occur but studies with various calcium channel blockers suggest that, in contrast to the response to potassium, a non-voltage sensitive calcium channel is involved. Other possible alternatives are discussed. As bradykinin stimulated an increase in inositol phosphate production, I attempted to measure the production of the other product of phospholipase C action on inositol phospholipids, diacylglycerol, in order to evaluate its possible role in the release response. This was attempted using both mass measurement, by the diacylglycerol kinase assay, and lipid labelling techniques. No increases in diacylglycerol in response to bradykinin were observed, even in the presence of inhibitors of diacylglycerol breakdown, which were able to increase basal diacylglycerol levels when added alone. These inhibitors, along with TPA, were used to evaluate the possible mechanism of action of protein kinase C in chromaffin cells, eg. feedback regulation or stimulation of release mechanisms. Failure to detect rises in diacylglycerol in response to bradykinin led to the final section of this work which looks at the production of one of the metabolic products of diacylglycerol breakdown, phosphatidic acid. Bradykinin is shown to stimulate a rapid, dose dependent increase in phosphatidic acid in chromaffin cells, which is, partially independent of extracellular calcium, independent of protein kinase C activation, and may be G-protein mediated. Studies of the route of formation of the phosphatidic acid show that phospholipase D is not involved and that inositol phospholipids or phosphatidylcholine are unlikely to be the main substrates for a phospholipase C mediated route, leaving the possibility of phospholipase C action on an alternative phospholipid. Finally the possible role of this production of phosphatidic acid in the chromaffin cell is discussed.
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Holz, Alexander. "Theoretische Untersuchungen zum Bindungsmodus nichtpeptidischer Bradykinin B2 Rezeptorantagonisten." [S.l.] : [s.n.], 2003. http://deposit.ddb.de/cgi-bin/dokserv?idn=968529038.

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Waldner, Maximilian. "Die Wirkung von Bradykinin auf die zerebrale Mikrozirkulation." Diss., lmu, 2007. http://nbn-resolving.de/urn:nbn:de:bvb:19-71745.

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Witherow, Fraser N. "Bradykinin : vasomotor tone and endogenous fibrinolysis in man." Thesis, University of Edinburgh, 2007. http://hdl.handle.net/1842/29426.

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Bradykinin is a nonapetide released into plasma during the contact phase of blood coagulation. It has a wide variety of physiological effects including vasodilatation, tissue-type plasminogen activator (t-PA) release, inflammatory mediator, ischaemic preconditioning and vasculogenesis. It is inactivated in plasma by angiotensinconverting enzyme (ACE). Inhibition of this enzyme has been shown to be beneficial in a variety of cardiovascular disorders including heart failure and hypertension, and it is clear that this benefit is not due entirely to reduction in the bioavailability of angiotensin II. We hypothesised that • bradykinin is a vasodilator and stimulates endothelial t-PA release via a specific receptor and that this effect is augmented by ACE inhibition. • in patients with heart failure, bradykinin contributes to peripheral and systemic vascular tone during treatment with ACE inhibition. Forearm blood flow was measured using bilateral forearm plethysmography during intrabrachial drug infusion. Bilateral venous cannulae were inserted to perform blood sampling for estimation of plasma t-PA and plasminogen activator inhibitor 1 (PAI- 1) concentrations. Cardiac output was measured with pulmonary artery catheterisation. The novel peptide bradykinin receptor antagonist, B9340, was used to oppose the effects of bradykinin. Studies were performed in healthy volunteers • to demonstrate the pharmacodynamics of B9340 and to demonstrate the selectivity of B9340 in opposing bradykinin-induced t-PA release. • to demonstrate the safety and tolerability of systemic intravenous B9340 administration. Studies were performed in patients with heart failure • to demonstrate the effect of ACE inhibition on endothelial t-PA release. • to demonstrate the effect of bradykinin antagonism on peripheral and systemic vascular tone in patients treated with ACE inhibition and angiotensin receptor blockade. Results In healthy volunteers • Bradykinin and substance P caused dose-dependent vasodilatation in the infused forearm (p < 0.001). B9340 caused a dose-dependent inhibition of bradykinin-induced forearm vasodilatation and t-PA release (p < 0.001) without affecting substance P-induced vasodilatation or t-PA release (p=NS). B9340 caused a reversible inhibition of bradykinin-induced vasodilatation (p < 0.001) with a rapid onset and offset of action. Intravenous systemic B9340 administration inhibited the local bradykinin-induced forearm vasodilatation in a dose-dependent manner. In patients with heart failure • bradykinin and substance P caused dose-dependent vasodilatation and release of t-PA from the infused forearm (p < 0.05). Long-term ACE inhibitor therapy caused an increase in forearm vasodilatation (p < 0.05) and t-PA release (p < 0.001) during bradykinin, but not substance P, infusion. • incremental doses of B9340 caused a dose-dependent reduction in forearm blood flow (p < 0.01). After withdrawal of ACE inhibitor therapy, B9340 produced no significant change in forearm blood flow. • systemic intravenous B9340 administration resulted in greater mean arterial pressure, systemic vascular resistance, pulmonary arterial wedge pressure, and mean pulmonary arterial pressure during ACE inhibitor therapy compared with losartan therapy (p < 0.005, p < 0.07, p < 0.0001, and p < 0.05 respectively) or placebo infusion (p < 0.005 for all). We have shown that bradykinin is a potent vasodilator that stimulates endogenous t-PA release and that these effects are receptor specific and can be blocked by a bradykinin receptor antagonist. We have also shown that bradykinin does not contribute to peripheral or systemic vascular tone in health but does contribute to peripheral and systemic vascular tone in patients with heart failure treated with chronic ACE inhibition. We believe this suggests that many of the beneficial actions of ACE inhibition are mediated through bradykinin.
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Blair, Alan. "Role of bradykinin in virus-induced airway inflammation." Thesis, Cardiff University, 2009. http://orca.cf.ac.uk/54363/.

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Asthma is a chronic inflammatory disease of the airways and viral infections account for the majority of exacerbations and may play a role in its pathogenesis. Bradykinin levels are increased in the lungs of asthmatics and inhaled bradykinin produces bronchoconstriction in asthmatic but not in normal patients. In this study, guinea-pigs were inoculated with parainfluenza and influenza virus to establish airways inflammation and hyperreactivity. The role of bradykinin in the parainfluenza model was examined by using the tissue kallikrein inhibitor, FE999024, and the bradykinin B2 receptor antagonist, MEN16132. Firstly, the effects of bradykinin inhalation in conscious guinea-pigs were characterized by using inhibitors of its breakdown and selective antagonists. Inhaled bradykinin produced a bronchoconstriction only after treatment with the inhibitors of angiotensin converting enzyme and/or neutral endopeptidase, captopril and phosphoramidon respectively. Inhaled bradykinin also increased inflammatory cell influx to the lungs when its breakdown was inhibited with both drugs. Cell influx and bronchoconstriction were blocked by the B2 receptor antagonists icatibant and MEN16132. These responses were therefore B2 receptor-mediated. In ovalbumin sensitized guinea-pigs, inhaled ovalbumin produced early and late asthmatic responses, inflammatory cell influx and airway hyperreactivity to histamine. These were inhibited by dexamethasone. Bradykinin caused bronchoconstriction without using metabolism inhibitors, indicating airways hyperreactivity to bradykinin. Parainfluenza-3 and influenza caused inflammatory cell influx and airways hyperreactivity to histamine. These were inhibited by FE999024, MEN16132 and dexamethasone. Parainfluenza-3 virus inoculated into sensitized guinea-pigs exacerbated the response to inhaled ovalbumin, with a prolonged bronchconstriction replacing early and late phases. This was resistant to dexamethasone. This study supports a role for bradykinin in virus-induced lung inflammation and the use of inhibitors of bradykinin for potential treatment of airway inflammation.
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Yang, M. "Catabolism and bioactivity of bradykinin and related peptides." Thesis, Queen's University Belfast, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.557857.

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Bradykinin and related peptides (BRPs) are common components of amphibian defensive skin secretions, particularly in ranid and phyllomedusine frogs and in bombinid toads. BRPs are known to be highly vasoactive with some possessing potent effects on blood vessel formation (angiogenesis) - a process known to be initiated by direct effects on endothelial cells. Human microvessel endothelial (HMEC) cells are a stable laboratory cell line often used for preliminary screening in such studies of BRP function. Since these cells are the starting points for fundamental biological studies, we examined their catabolism of bradykinin (BK) and maximakinin (MK). MK represents an N-terminally extended version of the former but with higher potency. Both BK and MK were broken down by proteases present on HMEC cells with half-lives of 5h and 2h, respectively. However, as two major metabolites of MK retained the receptor-active site of BK, the true half-life of non- active metabolite generation was 5h (BK) and 9h (MK). Bradykinin antagonists, kinestatin and QUB919, both from amphibian skin, were not degraded by HMEC cells and their presence did not interfere with the degradation of BK or MK. Using primer sets designed for bradykinin Bland B2 receptors, transcripts of appropriate size were amplified from an HMEC cell cDNA library. Bradykinin-related peptides are thus catabolised in different ways by HMEC cells and the cells were shown to contain polyadenylated mRNAs for both bradykinin receptor sub-types, Bland B2. To examine other functions of BRPs, we screened reverse phase HPLC fractions of venoms and defensive skin secretions to identify, structurally characterise and ultimately chemically-synthesise novel peptides to examine their effects on bradykinin activity using smooth muscle bioassays. Many BRPs exhibited anti- cancer and anti-microbial functions in our experiments giving us a broader perspective for further research in the BRP field. · ';.
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Polosa, Riccardo. "The mechanism of bradykinin-induced bronchoconstriction in asthma." Thesis, University of Southampton, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.295948.

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Ljunggren, Östen. "Involvement of bradykinin in inflammation induced bone resorption." Umeå : University of Umeå, 1991. http://catalog.hathitrust.org/api/volumes/oclc/24493228.html.

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Books on the topic "Bradykinin"

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1955-, Burch Ronald M., ed. Bradykinin antagonists: Basic and clinical research. New York: Dekker, 1991.

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Burch, Ronald M. Molecular biology and pharmacology of bradykinin receptors. Austin: R.G. Landes, 1993.

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Silva, M. Rocha e 1910- and Rothschild Adolfo Max, eds. Contributions to autacoid pharmacology: A festschrift in honour of Maurício Rocha e Silva. Basel: Birkhäuser Verlag, 1992.

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Keely, Stephen J. Regulation of colonic ion transport in vitro. Dublin: University College Dublin, 1995.

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Sharma, Jagdish N. Topics in mediator pharmacology. Hauppauge, N.Y: Nova Science Publishers, 2011.

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Ellard, John. Studies towards the synthesis of L-755,807: A novel, non-peptide bradykinin antagonist. [s.l.]: typescript, 2000.

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Tebbatt, Anne M. Studies towards the synthesis of the ring system of non-peptide bradykinin antagonist L-755,807, and its analogues. [s.l.]: typescript, 2000.

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1954-, Farmer Stephen G., ed. The Kinin system. San Diego: Academic Press, 1997.

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Reetz, Guido. Oszillation der cytosolischen Ca2-Aktivität und des Membranpotentials in Ratten-Gliomzellen und Astrozyten, ausgelöst durch Bradykinin und durch ATP. Magdeburg, Hecklinger Str. 29: G. Reetz, 1995.

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Verresen, L. Bradykinin. Leuven University Press, 1994.

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Book chapters on the topic "Bradykinin"

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Seth, John. "Bradykinin." In The Immunoassay Kit Directory, 26–27. Dordrecht: Springer Netherlands, 1994. http://dx.doi.org/10.1007/978-94-011-1414-1_7.

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Farmer, Stephen G. "Bradykinin." In Airways Smooth Muscle: Peptide Receptors, Ion Channels and Signal Transduction, 51–65. Basel: Birkhäuser Basel, 1995. http://dx.doi.org/10.1007/978-3-0348-7362-8_2.

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Gooch, Jan W. "Bradykinin." In Encyclopedic Dictionary of Polymers, 879. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-6247-8_13280.

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Sales, Vicência, and João Bosco Pesquero. "Bradykinin Receptors." In Encyclopedia of Signaling Molecules, 566–72. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_232.

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Saidak, Zuzana, Zakaria Ezzoukhry, Jean-Claude Maziere, Antoine Galmiche, Ken-Ichi Takemaru, Xingwang Chen, Feng-Qian Li, et al. "Bradykinin Receptors." In Encyclopedia of Signaling Molecules, 197–203. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_232.

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Vavrek, Raymond J., Lajos Gera, and John M. Stewart. "Pseudopeptide Analogs of Bradykinin and Bradykinin Antagonists." In Recent Progress on Kinins, 565–71. Basel: Birkhäuser Basel, 1992. http://dx.doi.org/10.1007/978-3-0348-7321-5_69.

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Floccard, Bernard, Jullien Crozon, Brigitte Coppere, Laurence Bouillet, and Bernard Allaouchiche. "Bradykinin-Mediated Angioedema." In Uncommon Diseases in the ICU, 175–90. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-04576-4_16.

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Inoki, R., and T. Kudo. "Bradykinin and enkephalins." In Dynamic Aspects of Dental Pulp, 385–401. Dordrecht: Springer Netherlands, 1990. http://dx.doi.org/10.1007/978-94-009-0421-7_25.

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Snyder, Solomon H., Donald C. Manning, and Larry R. Steranka. "Bradykinin and Pain." In Molecular and Cellular Aspects of the Drug Addictions, 92–110. New York, NY: Springer New York, 1989. http://dx.doi.org/10.1007/978-1-4613-8817-3_3.

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Floccard, B., E. Hautin, and B. Allaouchiche. "Bradykinin-mediated Angioedema." In Annual Update in Intensive Care and Emergency Medicine 2012, 504–15. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-25716-2_46.

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Conference papers on the topic "Bradykinin"

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Hewitt, Matthew M., and Brendan J. Canning. "MECHANISMS OF BRADYKININ EVOKED COUGH." 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.a5548.

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Kempe, S., J. Hahn, M. Jerg, C. Brunner, TK Hoffmann, and J. Greve. "Molecular mechanisms of bradykinin-induced angioedema." In Abstract- und Posterband – 89. Jahresversammlung der Deutschen Gesellschaft für HNO-Heilkunde, Kopf- und Hals-Chirurgie e.V., Bonn – Forschung heute – Zukunft morgen. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1639742.

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Marceau, François. "Maximakinin: An amphibian bradykinin homologue integrated into fusion proteins that bind to the bradykinin B2 receptor." In 7th International Electronic Conference on Medicinal Chemistry. Basel, Switzerland: MDPI, 2021. http://dx.doi.org/10.3390/ecmc2021-11403.

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Müller, E., A. Henschen, and G. Wunderer. "IDENTIFICATION OF A NEW HUMAN KININ, ILE-SER-BRADYKININ, BY HIGH-PERFORMANCE LIQUID CHROMATOGRAPHY AND SEQUENCE ANALYSIS IN OVARIAN CARCINOMA ASCITES." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642848.

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Human blood has been shown to contain two different kinin precursors, i.e0 the high and the low molecular mass kininogen0 These two kininogens release the same kinins, with the starting sequences Met-Lys-Arg-Pro-, Lys-Arg-Pro- or just Arg-Pro-depending on the releasing enzyme. The kinin starting with Arg-Pro- is denoted as bradykinin. In rats a different kininogen, called T-kininogen, is also present, especially as the major acute-phase protein in this species. The corresponding kinin, T-kinin, has the starting sequence Ile-Ser-Arg-Pro-. This type of kininogen or kinin has previously never been detected in human tissues. However, during the course of the present study evidence for existance of a third human kininogen, giving rise to human T-kinin, was obtained.Ascites from patients with metastatic ovarian carcinoma has been shown to contain high amounts of vascular permeability-increasing activity as determined by a rat skin-Evans blue test. When the ascites was fractionated by gel filtration followed by reversed-phase high-performance liquid chromatography (HPLC) a component could be isolated which by its total sequence and amino acid composition was identified as Ile-Ser-bradykinin. Several degradation products of this kinin were also detected as separate components in the chromatographies. The human Ile-Ser-bradykinin appeared on reversed-phase HPLC in the same position as synthetic T-kinin. It could be differentiated in this chromatography system from Met-Lys-bradykinin, Lys-bradykinin and bradykinin. It may be assumed that human Ile-Ser-bradykinin is released_ from a third, so far unidentified human kininogen which is only or predominantly expressed under certain pathophysiological conditions, and that therefore this new kinin might be employed as a tumor marker.
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Egberg, Nils, Krister Gréen, Jan Jacobsson, Ole Vester-gvist, Bjöm Wiman, and Michael Gallimore. "EFFECTS OF PLASMA KALLIKREIN AND BRADYKININ ON FIBRINOLYSIS AND THROMBOXANE PROSTACYKLIN FORMATION STUDIED IN MINIPIGS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644334.

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The effect of plasma kallikrein and bradykinin infusions into pigs on hemodynamic and hemostatic variables have been investigated. Both substances caused a pronounced decrease of the systemic blood pressure. The leucocyte count in periferal blood fell markedly, reaching a minimun within one hour after infusion of either of the substances.Signs that could be interpreted as a progressive disseminated intravascular coagulation with decrease of fibrinogen and platelet count was observed after kallikrein as well as bradykinin infusions. A pronounced increase of the plasma tissue plasminogen activator concentration followed both plasma kallikrein and bradykinin infusions. However, the peak concentration was found 5 minutes after bradykinin infusion but 60-120 minutes after kallikrein infusion, suggesting different mechanisms leading to the t-PA release. Concomittant with the maximun t-PA concentration there was a marked reduction of the plasminogen activator inhibitor (PAI) concentration. Three hours after drug infusions the PAI concentration was at or above preinfusion level. Kallikrein infusions caused a 10-20 fold increase of the urinary excretion of 2,3-dinor thromboxane B2 (metabolite of TxA2) and a 3-42 fold increase of 2,3-dinor-6-keto-PGFlalpha (metabolite of PGI2) excretion respectively. Corresponding data for bradykinin infusions were, 1.6-5 fold and 2-10 fold increases respectively. Possible links between leucocyte aggregation, prostanoid formation and fibrinolytic variables will be discussed.
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Lee, Yeon Sun, Sara M. Hall, Cyf Ramos-Colon, Dhana Muthu, David Rankin, Frank Porreca, Josephine Lai, and Victor J. Hruby. "[Des-Arg7]-Dynorphin A Analogs for Bradykinin-2 Receptor." In The Twenty-Third American and the Sixth International Peptide Symposium. Prompt Scientific Publishing, 2013. http://dx.doi.org/10.17952/23aps.2013.134.

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Lopes, Flavio A., Jones M. Silva, Maria Luiza V. Oliva, and Antonio Miranda. "Bauhinia Bauhinioides Kallikrein Inhibitor Fragments with Bradykinin-Like Activities." In The 24th American Peptide Symposium. Prompt Scientific Publishing, 2015. http://dx.doi.org/10.17952/24aps.2015.082.

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Hahn, J., M. Nordmann, TK Hoffmann, J. Greve, B. Bock, A. Pfaue, and CM Muth. "Ulmer Notfallalgorithmus: Therapie von Medikamenten-induzierten, Bradykinin vermittelten Angioödemen." In Abstract- und Posterband – 89. Jahresversammlung der Deutschen Gesellschaft für HNO-Heilkunde, Kopf- und Hals-Chirurgie e.V., Bonn – Forschung heute – Zukunft morgen. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1639735.

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Yu, Hsin-Shan, and Chih-Hsin Tang. "Abstract 1396: Bradykinin enhances cell migration in human prostate carcinoma cells via bradykinin B2 receptor, PKCdelta, c-Src and NF-kappaB signaling pathways." 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.am2011-1396.

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Keir, Sandra, Domenico Spina, and Clive Page. "Platelet Involvement In Bradykinin-Induced Airways Obstruction In Guinea Pigs." 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.a2141.

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