Log in

Relevant bibliographies by topics / Bradykinine / Journal articles

To see the other types of publications on this topic, follow the link: Bradykinine.

Journal articles on the topic 'Bradykinine'

Author: Grafiati

Published: 4 June 2021

Last updated: 18 February 2022

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the top 50 journal articles for your research on the topic 'Bradykinine.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.

1

Bascands, JL, and JP Girolami. "La bradykinine." médecine/sciences 12, no. 5 (1996): 582. http://dx.doi.org/10.4267/10608/787.

Full text

APA, Harvard, Vancouver, ISO, and other styles

2

Buléon, Marie, Marion Mehrenberger, Christiane Pécher, et al. "Bradykinine et néphroprotection." médecine/sciences 23, no. 12 (2007): 1141–47. http://dx.doi.org/10.1051/medsci/200723121141.

Full text

APA, Harvard, Vancouver, ISO, and other styles

3

Du-Thanh, A., N. Raison-Peyron, and B. Guillot. "Les angioedèmes à bradykinine." Annales de Dermatologie et de Vénéréologie 138, no. 4 (2011): 328–35. http://dx.doi.org/10.1016/j.annder.2010.12.017.

Full text

APA, Harvard, Vancouver, ISO, and other styles

4

Du-Thanh, A., N. Raison-Peyron, and B. Guillot. "Les angiœdèmes à bradykinine." Annales de Dermatologie et de Vénéréologie 138, no. 4 (2011): 336. http://dx.doi.org/10.1016/j.annder.2011.01.020.

Full text

APA, Harvard, Vancouver, ISO, and other styles

5

Du-Thanh, A., N. Raison-Peyron, and B. Guillot. "Les angiœdèmes à bradykinine." Annales de Dermatologie et de Vénéréologie 138, no. 4 (2011): 327. http://dx.doi.org/10.1016/j.annder.2011.01.021.

Full text

APA, Harvard, Vancouver, ISO, and other styles

6

Dusser, D. "Hyperréactivité bronchique et bradykinine : perspectives thérapeutiques." Revue Française d'Allergologie et d'Immunologie Clinique 38, no. 10 (1998): 690–92. http://dx.doi.org/10.1016/s0335-7457(98)80172-x.

Full text

APA, Harvard, Vancouver, ISO, and other styles

7

Bascands, Jean-Loup, Joost P. Schanstra, Réjean Couture, and Jean-Pierre Girolami. "Les récepteurs de la bradykinine : de nouveaux rôles physiopathologiques." médecine/sciences 19, no. 11 (2003): 1093–100. http://dx.doi.org/10.1051/medsci/200319111093.

Full text

APA, Harvard, Vancouver, ISO, and other styles

8

Floccard, B., J. Crozon, T. Rimmelé, et al. "Prise en charge en urgence de l’angiœdème à bradykinine." Annales Françaises d'Anesthésie et de Réanimation 30, no. 7-8 (2011): 578–88. http://dx.doi.org/10.1016/j.annfar.2011.01.011.

Full text

APA, Harvard, Vancouver, ISO, and other styles

9

Coquart, N., A. M. Roguedas, C. Abasq, and L. Misery. "Urticaire superficielle au cours des angio-œdèmes à bradykinine." Annales de Dermatologie et de Vénéréologie 139, no. 12 (2012): B205. http://dx.doi.org/10.1016/j.annder.2012.10.347.

Full text

APA, Harvard, Vancouver, ISO, and other styles

10

Woodley, N., and J. K. Barclay. "Cultured endothelial cells from distinct vascular areas show differential responses to agonists." Canadian Journal of Physiology and Pharmacology 72, no. 9 (1994): 1007–12. http://dx.doi.org/10.1139/y94-140.

Full text

Abstract:

Nous avons comparé la capacité des cellules endothéliales isolées de l'aorte, de la veine cave, de la chambre ventriculaire et du système microvasculaire pulmonaire du lapin de produire un ou des facteurs de relaxation en réponse à l'acetylcholine (ACh) et à la bradykinine (BK). Des anneaux aortiques de lapin dépouillés d'endothélium ont été précontractés avec 1 μM de phényléphrine et superfusés à 2 mL/min avec une solution tampon bicarbonatée de Krebs–Henseleit. Les anneaux ont été exposées à des épreuves témoins d'embols de 3 mL de 1 μM d'ACh ou 1 μM de BK. Les embols d'ACh et de BK ont été

APA, Harvard, Vancouver, ISO, and other styles

11

Bouillet, L. "L’angiœdème laryngé induit par les médicaments interférant avec le métabolisme de la bradykinine." Revue Française d'Allergologie 52, no. 3 (2012): 157–59. http://dx.doi.org/10.1016/j.reval.2012.01.006.

Full text

APA, Harvard, Vancouver, ISO, and other styles

12

Charignon, D., A. Ghannam, F. Defendi, et al. "Facteurs modificateurs des angiœdèmes héréditaires à bradykinine (AOH): différences selon le type d’angiœdème." Revue Française d'Allergologie 55, no. 3 (2015): 237. http://dx.doi.org/10.1016/j.reval.2015.02.081.

Full text

APA, Harvard, Vancouver, ISO, and other styles

13

Bohlender, J., J. Nussberger, C. Amstutz, F. Birkhäuser, G. N. Thalmann, and H. Imboden. "La dénervation rénale unilatérale et le système kallikréine-bradykinine rénal chez le rat." Annales de Cardiologie et d'Angéiologie 62, no. 3 (2013): 144–48. http://dx.doi.org/10.1016/j.ancard.2013.04.014.

Full text

APA, Harvard, Vancouver, ISO, and other styles

14

Moriceau, F., B. Floccard, O. Martin, et al. "Angiœdèmes à bradykinine : les traitements efficaces existent, il faudrait pouvoir en disposer vite !" Annales Françaises d'Anesthésie et de Réanimation 33 (September 2014): A346—A347. http://dx.doi.org/10.1016/j.annfar.2014.07.589.

Full text

APA, Harvard, Vancouver, ISO, and other styles

15

Defendi, F., D. Charignon, A. Ghannam, et al. "Méthodes d’identification de l’angiœdème à bradykinine (AOBK) : application aux patients pour une typologie avancée." Revue Française d'Allergologie 55, no. 3 (2015): 233. http://dx.doi.org/10.1016/j.reval.2015.02.072.

Full text

APA, Harvard, Vancouver, ISO, and other styles

16

Hofman, Z. L., A. Relan, S. Zeerleede, C. Drouet, B. Zuraw, and E. Hack. "Manifestations locales au cours d’un processus systémique : modèle pathogénique de l’angiœdème à bradykinine (AOBK)." Revue Française d'Allergologie 55, no. 3 (2015): 264–65. http://dx.doi.org/10.1016/j.reval.2015.02.158.

Full text

APA, Harvard, Vancouver, ISO, and other styles

17

Ruiz, S., V. Merlet-Dupuy, M. Buléon, et al. "Le récepteur B1 de la bradykinine : cible thérapeutique potentielle de l’hyperperméabilité vasculaire du sepsis." Annales Françaises d'Anesthésie et de Réanimation 33 (September 2014): A105. http://dx.doi.org/10.1016/j.annfar.2014.07.173.

Full text

APA, Harvard, Vancouver, ISO, and other styles

18

Defendi, F., D. Charignon, A. Ghannam, et al. "Intérêt de l’étude du métabolisme de la bradykinine (BK) pour la prise en charge des angioedèmes." Annales de Dermatologie et de Vénéréologie 140, no. 12 (2013): S386—S387. http://dx.doi.org/10.1016/j.annder.2013.09.057.

Full text

APA, Harvard, Vancouver, ISO, and other styles

19

Meyer, Richard A., and Karen A. Davis. "Een sympathectomie bij de mens leidt niet tot verdwijning van een door bradykinine opgewekte cutane hyperalgesie." Stimulus 13, no. 4 (1994): 279. http://dx.doi.org/10.1007/bf03075949.

Full text

APA, Harvard, Vancouver, ISO, and other styles

20

Serres-Cousiné, A., A. Du-Thanh, N. Raison-Peyron, and B. Guillot. "Un cas d’angioedème à bradykinine sous inhibiteur de l’enzyme de conversion aggravé par la prise de gliptine." Annales de Dermatologie et de Vénéréologie 138, no. 12 (2011): A272—A273. http://dx.doi.org/10.1016/j.annder.2011.10.351.

Full text

APA, Harvard, Vancouver, ISO, and other styles

21

Serres-Cousiné, A., A. Du Thanh, B. Guillot, and N. Raison-Peyron. "Angiœdèmes à bradykinine sous inhibiteurs de l’enzyme de conversion, sartans et gliptines : étude rétrospective chez 37 patients." Annales de Dermatologie et de Vénéréologie 139, no. 12 (2012): B125—B126. http://dx.doi.org/10.1016/j.annder.2012.10.168.

Full text

APA, Harvard, Vancouver, ISO, and other styles

22

Bouillet, L., I. Boccon-Gibod, D. Ponard, et al. "L’icatibant (antagoniste des récepteurs B2 de la Bradykinine) est efficace dans le traitement des angioedèmes héréditaires de type III." La Revue de Médecine Interne 30 (December 2009): S461. http://dx.doi.org/10.1016/j.revmed.2009.10.375.

Full text

APA, Harvard, Vancouver, ISO, and other styles

23

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

24

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

25

Dabire, H., S. Blot, I. Barthelemy, et al. "H018 L’administration chronique de bradykinine restaure la fonction endothéliale vasculaire dans un modèle canin de la dystrophie musculaire de duchenne." Archives of Cardiovascular Diseases 102 (March 2009): S78. http://dx.doi.org/10.1016/s1875-2136(09)72317-4.

Full text

APA, Harvard, Vancouver, ISO, and other styles

26

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

27

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

28

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

29

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 (2001): 651–57. http://dx.doi.org/10.1042/cs1010651.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

30

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

31

Zarubina, Irina V., and Petr D. Shabanov. "From the S.P. Botkin’s idea of “preexposure” to preconditioning phenomenon. Perspectives for use of phenomena of ischemic and pharmacological preconditioning." Reviews on Clinical Pharmacology and Drug Therapy 14, no. 1 (2016): 4–28. http://dx.doi.org/10.17816/rcf1414-28.

Full text

Abstract:

The phenomenon of ischemic preconditioning based on the S.P. Botkin’s idea about defense effect of disturbing factors acting in small intensities is observed in the review. The modern literature data about main types of preconditioning exposure, triggers and mechanisms of ischemic preconditioning are reviewed. This phenomenon was supported in many experiments in vivo and in vitro on animals of different spices as well as in humans in clinical conditions. Ischemic preconditioning is qualified as transient positive changes in the organs and tissues produced by activation of rapid endogenous adop

APA, Harvard, Vancouver, ISO, and other styles

32

Charbonneau, Hélène, Nicolas Mayeur, Marie Buléon, et al. "Le blocage du récepteur B2 de la bradykinine permet de prévenir les effets hypotenseurs des inhibiteurs de l’enzyme de conversion au cours d’un choc hémorragique contrôlé." Anesthésie & Réanimation 1 (September 2015): A67—A68. http://dx.doi.org/10.1016/j.anrea.2015.07.104.

Full text

APA, Harvard, Vancouver, ISO, and other styles

33

Krieg, Thomas, Qining Qin, Sebastian Philipp, Mikhail F. Alexeyev, Michael V. Cohen, and James M. Downey. "Acetylcholine and bradykinin trigger preconditioning in the heart through a pathway that includes Akt and NOS." American Journal of Physiology-Heart and Circulatory Physiology 287, no. 6 (2004): H2606—H2611. http://dx.doi.org/10.1152/ajpheart.00600.2004.

Full text

Abstract:

In the rabbit heart, bradykinin and ACh trigger preconditioning by a mechanism involving ATP-sensitive potassium channel-dependent production of reactive oxygen species (ROS). Recent evidence indicates that the pathway by which bradykinin causes ROS generation includes nitric oxide synthase (NOS) and protein kinase G (PKG). On the other hand, Akt was shown to be essential for ACh to generate ROS. This study determines whether these two G-coupled receptor agonists indeed have similar signaling targets, i.e., whether Akt is involved in bradykinin's pathway and whether NOS is involved in ACh's pa

APA, Harvard, Vancouver, ISO, and other styles

34

Olson, K. R., D. J. Conklin, L. Weaver, et al. "Cardiovascular effects of homologous bradykinin in rainbow trout." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 272, no. 4 (1997): R1112—R1120. http://dx.doi.org/10.1152/ajpregu.1997.272.4.r1112.

Full text

Abstract:

Bradykinins have only recently been identified in fish, and a detailed analysis of their cardiovascular actions is lacking. The present study examines the cardiovascular effects of trout bradykinin ([Arg0,Trp5,Leu8]bradykinin; tBK) in conscious trout, Oncorhynchus mykiss. tBK (1-10 nmol/kg body wt bolus) produced triphasic pressor-depressor-pressor responses. In phase 1, cardiac output (CO), ventral aortic (P(VA)), dorsal aortic (P(DA)), and central venous pressure increased, whereas systemic (R(S)) and gill resistance (R(G)) were unchanged. In phase 2, R(G) increased, whereas R(S), CO, and he

APA, Harvard, Vancouver, ISO, and other styles

35

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.

Full text

Abstract:

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 co

APA, Harvard, Vancouver, ISO, and other styles

36

Leong, Patrick K. K., Yibin Zhang, Li E. Yang, Niels-Henrik Holstein-Rathlou, and Alicia A. McDonough. "Diuretic response to acute hypertension is blunted during angiotensin II clamp." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 283, no. 4 (2002): R837—R842. http://dx.doi.org/10.1152/ajpregu.00089.2002.

Full text

Abstract:

Acute hypertension inhibits proximal tubule (PT) fluid reabsorption. The resultant increase in end proximal flow rate provides the error signal to mediate tubuloglomerular feedback autoregulation of renal blood flow and glomerular filtration rate and suppresses renal renin secretion. To test whether the suppression of the renin-angiotensin system during acute hypertension affects the magnitude of the inhibition of PT fluid and sodium reabsorption, plasma ANG II levels were clamped by infusion of the angiotensin-converting enzyme (ACE) inhibitor captopril (12 μg/min) and ANG II after pretreatme

APA, Harvard, Vancouver, ISO, and other styles

37

Chen, Zu-Lin, Pradeep Singh, Jyen Wong, Katharina Horn, Sidney Strickland та Erin H. Norris. "An antibody against HK blocks Alzheimer’s disease peptide β-amyloid−induced bradykinin release in human plasma". Proceedings of the National Academy of Sciences 116, № 46 (2019): 22921–23. http://dx.doi.org/10.1073/pnas.1914831116.

Full text

Abstract:

Bradykinin is a proinflammatory factor that mediates angioedema and inflammation in many diseases. It is a key player in some types of hereditary angioedema and is involved in septic shock, traumatic injury, Alzheimer’s disease (AD), and stroke, among others. Activation of the plasma contact system leads to elevated levels of plasma kallikrein, which cleaves high molecular weight kininogen (HK) to release bradykinin. Drug development for bradykinin-meditated pathologies has focused on designing inhibitors to the enzymes that cleave HK (to prevent bradykinin release) or antagonists of endotheli

APA, Harvard, Vancouver, ISO, and other styles

38

Duncan, Ann-Maree, Athena Kladis, Garry L. Jennings, Anthony M. Dart, Murray Esler, and Duncan J. Campbell. "Kinins in humans." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 278, no. 4 (2000): R897—R904. http://dx.doi.org/10.1152/ajpregu.2000.278.4.r897.

Full text

Abstract:

The kinin peptide system in humans is complex. Whereas plasma kallikrein generates bradykinin peptides, glandular kallikrein generates kallidin peptides. Moreover, a proportion of kinin peptides is hydroxylated on proline3 of the bradykinin sequence. We established HPLC-based radioimmunoassays for nonhydroxylated and hydroxylated bradykinin and kallidin peptides and their metabolites in blood and urine. Both nonhydroxylated and hydroxylated bradykinin and kallidin peptides were identified in human blood and urine, although the levels in blood were often below the assay detection limit. Whereas

APA, Harvard, Vancouver, ISO, and other styles

39

HARVEY, Justine S., and Gillian M. BURGESS. "Cyclic GMP regulates activation of phosphoinositidase C by bradykinin in sensory neurons." Biochemical Journal 316, no. 2 (1996): 539–44. http://dx.doi.org/10.1042/bj3160539.

Full text

Abstract:

Prior exposure of cultured neonatal rat dorsal root ganglion (DRG) neurons to bradykinin resulted in marked attenuation of bradykinin-induced activation of phosphoinositidase C (PIC). The (logconcentration)–response curve for bradykinin-induced [3H]inositol trisphosphate ([3H]IP3) formation was shifted to the right and the maximum response was reduced. Bradykinin increases cyclic GMP (cGMP) in DRG neurons [Burgess, Mullaney, McNeill, Coote, Minhas and Wood (1989) J. Neurochem. 53, 1212–1218] and treatment of the neurons with dibutyryl cGMP (dbcGMP) had a similar, inhibitory, effect on bradykin

APA, Harvard, Vancouver, ISO, and other styles

40

McAllister, B. S., F. Leeb-Lundberg, and M. S. Olson. "Bradykinin inhibition of EGF- and PDGF-induced DNA synthesis in human fibroblasts." American Journal of Physiology-Cell Physiology 265, no. 2 (1993): C477—C484. http://dx.doi.org/10.1152/ajpcell.1993.265.2.c477.

Full text

Abstract:

Bradykinin exhibits proliferative influences in several types of cells; however, in the present study, bradykinin did not promote DNA synthesis but actually inhibited the DNA synthesis induced by epidermal growth factor (EGF) and platelet-derived growth factor (PDGF) in human gingival fibroblasts (HGF). This dose-dependent inhibitory effect was a specific intracellular interaction in that increasing concentrations of EGF did not counteract the inhibitory actions of bradykinin when added at 100 nM. The phosphoinositide-calcium signaling cascade is a likely point of interaction for the inhibitor

APA, Harvard, Vancouver, ISO, and other styles

41

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

42

Grafe, M., C. Bossaller, K. Graf, et al. "Effect of angiotensin-converting-enzyme inhibition on bradykinin metabolism by vascular endothelial cells." American Journal of Physiology-Heart and Circulatory Physiology 264, no. 5 (1993): H1493—H1497. http://dx.doi.org/10.1152/ajpheart.1993.264.5.h1493.

Full text

Abstract:

The degradation of bradykinin by angiotensin-converting-enzyme (ACE) activity in cultured human endothelial cells was studied by direct measurement of bradykinin and by its effect on the release of endothelium-derived relaxing factors. The half-life of exogenous bradykinin (10,000 pg/ml) was calculated from the decay of the bradykinin concentration as 46 +/- 2 min in cell monolayers, 133 +/- 15 min in conditioned medium, and 24 +/- 2 min in homogenates. Most of the bradykinin-degrading activity in cell monolayers could be inhibited in a concentration-dependent manner by the ACE inhibitors lisi

APA, Harvard, Vancouver, ISO, and other styles

43

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

44

Kajekar, Radhika, and Allen C. Myers. "Effect of bradykinin on membrane properties of guinea pig bronchial parasympathetic ganglion neurons." American Journal of Physiology-Lung Cellular and Molecular Physiology 278, no. 3 (2000): L485—L491. http://dx.doi.org/10.1152/ajplung.2000.278.3.l485.

Full text

Abstract:

The effect of bradykinin on membrane properties of parasympathetic ganglion neurons in isolated guinea pig bronchial tissue was studied using intracellular recording techniques. Bradykinin (1–100 nM) caused a reversible membrane potential depolarization of ganglion neurons that was not associated with a change in input resistance. The selective bradykinin B2 receptor antagonist HOE-140 inhibited bradykinin-induced membrane depolarizations. Furthermore, the cyclooxygenase inhibitor indomethacin attenuated bradykinin-induced membrane depolarizations to a similar magnitude (∼70%) as HOE-140. Howe

APA, Harvard, Vancouver, ISO, and other styles

45

Berman, A. R., A. G. Togias, G. Skloot, and D. Proud. "Allergen-induced hyperresponsiveness to bradykinin is more pronounced than that to methacholine." Journal of Applied Physiology 78, no. 5 (1995): 1844–52. http://dx.doi.org/10.1152/jappl.1995.78.5.1844.

Full text

Abstract:

Bradykinin reduces airflow in asthmatic patients via indirect mechanism(s), possibly involving sensory nerve stimulation and increased vascular permeability. We hypothesized that allergen inhalation, which affects reactivity of nerves and vessels, would differentially alter reactivity to bradykinin and the smooth muscle spasmogen methacholine. We compared reactivity to methacholine and bradykinin 1, 2, 4, 7, 11, and 14 days after allergen provocation in 12 atopic asthmatic patients with stable baseline reactivity to bradykinin. Maximal allergen-induced shifts from baseline in reactivity were 0

APA, Harvard, Vancouver, ISO, and other styles

46

Bertrand, C., P. Geppetti, J. Baker, G. Petersson, G. Piedimonte, and J. A. Nadel. "Role of peptidases and NK1 receptors in vascular extravasation induced by bradykinin in rat nasal mucosa." Journal of Applied Physiology 74, no. 5 (1993): 2456–61. http://dx.doi.org/10.1152/jappl.1993.74.5.2456.

Full text

Abstract:

We used Evans blue dye to assess the effects of bradykinin on vascular extravasation in nasal mucosa of pathogen-free F344 rats. There was a dose-dependent increase in Evans blue extravasation when bradykinin was delivered by topical instillation in the nose (doses, 25–100 nmol). Only the highest intravenous doses (2 and 5 mumol/kg) of bradykinin caused increased extravasation. When bradykinin was delivered by either route, its effect on extravasation was exaggerated by pharmacological inhibition of the enzymes neutral endopeptidase (NEP) and kininase II [angiotensin-converting enzyme (ACE)].

APA, Harvard, Vancouver, ISO, and other styles

47

SCHANSTRA, JOOST P., MARIA E. MARIN-CASTAÑO, FRANÇOISE PRADDAUDE, et al. "Bradykinin B1Receptor-Mediated Changes in Renal Hemodynamics during Endotoxin-Induced Inflammation." Journal of the American Society of Nephrology 11, no. 7 (2000): 1208–15. http://dx.doi.org/10.1681/asn.v1171208.

Full text

Abstract:

Abstract. Kinins have been shown to influence renal hemodynamics and function. Under physiologic conditions, most kinin effects involve bradykinin B2receptors, but bradykinin B1receptors are often induced during inflammation. The purpose of this study was to examinein vivothe effects of bradykinin B1receptor activation on renal hemodynamics under normal and inflammatory conditions. In anesthetized rats, activation of bradykinin B1receptors by arterial infusion of bradykinin B1receptor agonist des-Arg9-bradykinin reduced renal plasma flow and GFR. Prior administration (18 h) of lipopolysacchari

APA, Harvard, Vancouver, ISO, and other styles

48

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

49

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.

Full text

Abstract:

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.

APA, Harvard, Vancouver, ISO, and other styles

50

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!