Wyniki wyszukiwania - Biblioteka Nauki

1

New bradykinin analogues acylated on the N-terminus: effect on rat uterus and blood pressure

100%

Labudda O. , Wierzba T. , Sobolewski D. , Śleszyńska M. , Gawiński Ł. , Plackova M. , Slaninová J. , Prahl A.

Acta Biochimica Polonica

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2007

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tom 54

|

nr 1

193-198

EN

Our previous studies suggested that acylation of the N-terminus of several known B2 antagonists with various kinds of bulky acyl groups consistently improved their antagonistic potency in rat blood pressure assay. On the other hand, our earlier observations also seemed to suggest that the effects of acylation on the contractility of isolated rat uterus depended substantially on the chemical character of the acyl group, as we observed that this modification might either change the range of antagonism or even transform it into agonism. Bearing all this in mind, we decided to synthesize seven new analogues of bradykinin by N-terminal acylation with various acyl groups of a moderately potent B2 antagonist, previously synthesized by Stewart's group, D-Arg-Arg-Pro-Hyp-Gly-Thr-Ser-D-Phe-Thi-Arg. The analogues were tested in vitro for their blood pressure-lowering and uterotonic activities. The modifications either preserved or increased the antagonistic potency in the rat blood pressure test. On the other hand, all seven substituents negatively influenced the interaction with the rat uterine receptors. Our results may be helpful for designing new B2 agonists and antagonists.

2

New Bradykinin Analogues Modified in Position 6 and 7 with Naphthylalanine

100%

Prahl A. , Derdowska I. , Dawidowska O. , Neubert K. , Hartrodt B. , Wierzba T. , Juzwa W. , Lammek B.

Polish Journal of Chemistry

|

2003

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tom Vol. 77 / nr 7

881-887

EN

We describe the synthesis and some pharmacological properties of eight new analogues of a previously synthesized bradykinin antagonist, D-Arg-Arg-Pro-Hyp-Gly-Thi-Ser- D-Phe-Thi-Arg. Two peptides were designed by substitution of Ser6 with L-1- and L-2-naphthylalanine. In two further analogues this modification was combined with placement in position 7 of D-naphthylalanine residue. We also obtained four analogues by acylation of N-terminus of the peptides mentioned above with 1-adamantaneacetic acid. The activity of analogues was assessed by their ability to inhibit vasodepressor response to exogenous bradykinin (rat blood pressure test). Our results indicate that the modifications proposed decreased significantly the B2 antagonistic activity. Moreover, our earlier observation, suggesting that acylation of the N-terminus of many BK antagonists with bulky groups consistently improved the antagonistic potency, appears to be valid only for one pair of analogues.

3

New Analogues of Bradykinin Substituted in the C-Terminal Part of the Molecule with Naphthylalanine

100%

Prahl A. , Derdowska I. , Dawidowska O. , Neubert K. , Hartrodt B. , Wierzba T. , Juzwa W. , Lammek B.

Polish Journal of Chemistry

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2002

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tom Vol. 76 / nr 10

1433-1439

EN

This paper describes the synthesis and some pharmacological properties of eight new analogues of a previously synthesized bradykinin antagonist, D-Arg-Arg-Pro-Hyp-Gly- Thi-Ser-D-Phe-Thi-Arg. Two peptides were designed by substitution of Thi8 with L-1- and L-2-naphthylalanine. In two further analogues this modification was combined with placement in position 7 of D-2-naphthylalanine residue. Finally, we obtained four analogues by acylation of N-terminus of the peptides mentioned above with 1-adamantaneacetic acid. The activity of analogues was assessed by their ability to inhibit vasodepressor response to exogenous bradykinin (rat blood pressure test). Our results indicate that the modification proposed decreased the B2 antagonistic activity, however, the range of this effect was different. We also observed that even minor changes in the structure of the C-terminal part of the B2 antagonists may significantly influence their activity.

4

New bradykinin Analogues Substituted in Positions 6 and 7 with Enantiomers of N-Methylphenylalanine

100%

Wierzba T. , Derdowska I. , Juzwa W. , Neubert K. , Hartrodt B. , Lammek B.

Polish Journal of Chemistry

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2002

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tom Vol. 76 / nr 5

713-719

EN

Four new analogues of a previously designed bradykinin antagonist, D-Arg-Arg-Pro- -Hyp-Gly-Thi-Ser-D-Phe-Thi-Arg, containing replacements in positions 6 and 7 with all possible combinations of enantiomers of N-methylphenylalanine (MePhe) were designed, synthesized and bioassayed. The presence of two consecutive MePhe residues in the sequence of the analogues caused great difficulties in the synthesis. The best results for the CO-N(CH3) bond formation were obtained using O-(7-azabenzotriazol-1-yl)-1,1,3,3- -tetramethyluronium hexafluorophosphate/7-azabenzotriazol-1-ol (HATU/HOAt) as coupling reagent (Fmoc strategy). The antagonistic potency of these peptides was assessed by their ability to inhibit vasodepressor response to exogenous bradykinin in conscious rats. Our results showed that the modifications proposed resulted in a decrease in antagonistic activity. However, we demonstrated once again that the D-amino acid in position 7 ofBKantagonists may be replaced by a suitable L-amino acid residue. Our results may be of value in the design of new B2-antagonists.

5

Metabolism of bradykinin in aorta of hypertensive rats

100%

Bujak-Giżycka B. , Olszanecki R. , Madej J. , Suski M. , Gębska A. , Korbut R.

Acta Biochimica Polonica

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2011

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tom 58

|

nr 2

199-202

EN

Alterations in the formation and metabolism of bradykinin (Bk) are hypothesized to play a role in the pathophysiology of hypertension, atherosclerosis and vascular complications of diabetes. However, despite its prominent role in cardiovascular regulation, studies on bradykinin have been limited by various difficulties in accurate measurements of this peptide in biological samples. In this study, using the LC-ESI-MS method we estimated the conversion of exogenous Bk to its main metabolites - Bk-(1-5) and Bk-(1-7) - in endothelial cell culture and in fragments of aorta of normotensive (WKY) and hypertensive rats (SHR). The effects of angiotensin converting enzyme (ACE) and neutral endopeptidase (NEP) inhibitors were more pronounced in SHR: perindoprilat inhibited Bk-(1-5) formation by 49 % and 76 % in WKY and SHR rats, respectively, and tiorphan tended to decrease formation of Bk-(1-5) in both groups of animals. The degradation of bradykinin and generation of both metabolites were significantly higher in the aorta of SHR rats than in WKY controls. Our results show that even in relatively early hypertension (in 4-month old SHR rats) inactivation of Bk by aorta wall is enhanced.

6

Bradykinin B2 receptor and dopamine D2 receptor cooperatively contribute to the regulation of neutrophil adhesion to endothelial cells

88%

Niewiarowska-Sendo A. , Łabędź-Masłowska A. , Kozik A. , Guevara-Lora I.

Acta Biochimica Polonica

|

2018

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tom 65

|

nr 3

367-375

EN

Leukocyte adhesion to the vascular endothelium contributes to many immunological and inflammatory disorders. These processes have been shown to be mediated by bradykinin receptor type 2 (B2R) and dopamine receptor type 2 (D2R). In a previous study, we reported the formation of a B2R-D2R heterodimer, possibly altering cellular functions. Hence, in the present study, we examined the effect of co-activation of endothelial cells with B2R and D2R agonists on the interaction of these cells with neutrophils. Bradykinin, the main B2R agonist, significantly increased cell adhesion, and this effect was reversed when the endothelial cells were additionally co-treated with a selective D2R agonist, sumanirole. These results were dependent on the incubation time, showing an opposite tendency after prolonged stimulation. Significant changes in the expression of adhesion proteins, such as E-selectin and intercellular adhesion molecule 1 in endothelial cells were observed. Additionally, the cells preincubated with tumor necrosis factor-α showed decreased cell adhesion and IL-8 release after long incubation with both agonists. The modulation of cell adhesion by D2R and B2R seem to be mediated via STAT3 phosphorylation. In summary, this study demonstrated a protective role of D2R in neutrophil-endothelial cell adhesion induced by bradykinin, especially in cytokine-stimulated endothelial cells.

7

New bradykinin B2 receptor antagonists - influence of C-terminal segment modifications on their pharmacological properties

88%

Śleszyńska M. , Kwiatkowska A. , Sobolewski D. , Wierzba T. , Katarzyńska J. , Zabrocki J. , Borovickova L. , Slaninová J. , Prahl A.

Acta Biochimica Polonica

|

2009

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tom 56

|

nr 4

641-648

EN

In the present study we describe the synthesis and some pharmacological properties of eight new analogues of bradykinin (BK). Two peptides were designed by substitution of position 7 or 8 of the known [d-Arg0,Hyp3,Thi5,8,d-Phe7]BK antagonist (Stewart's antagonist) with l-pipecolic acid (l-Pip). The next two analogues were obtained by replacement of the d-Phe residue in position 7 of the Stewart's peptide with l-β2-isoproline (l-β2-iPro) or l-β3-homoproline (l-β3-hPro). The four analogues mentioned above were also prepared in N-acylated form with 1-adamantaneacetic acid (Aaa). Biological activity of the compounds was assessed by isolated rat uterus and rat blood pressure tests. Our results showed that l-Pip in position 7 slightly increased antagonistic potency in the blood pressure test, but it turned the analogue into an agonist in the rat uterus test. Replacement of Thi by l-Pip in position 8 also enhanced antagonism in the rat pressure test but preserved the antagonism in the rat uterus test. l-β2-iPro or l-β3-hPro in position 7 decreased the potencies in both tests. We also demonstrated that acylation of the N-terminus did not increase, as was claimed previously, the antagonistic potencies of the resulting peptides. The results thus support the hypothesis about the existence of different types of BK receptors in the rat uterus and blood vessels. Our studies provide new information about the structure-activity relationship of BK antagonists which may help in designing more potent BK receptor blockers.

8

Kallikrein-thrombolytic and hypotensive action in cats - preliminary results

75%

Swies J. , Grodzinska L. , Slawinski M. , Gryglewski R. J.

Acta Physiologica Polonica

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1990

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tom 41

|

nr 1-3

EN

Święs J., Grodzińska L., Sławiński M., Gryglewski R. J.: Kallikrein-thrombolytic and hypotensive action in cats - preliminary results. Acta Physiol. Pol. 1990, 41 (1-3): 87-95. An intravenous injection of kallikrein produced hypotensive and thrombolytic effects in anasthetized cats, using the blood superfused tendon technique. The thrombolytic action of kallikrein was mediated by an unstable substance. The generation of this substance was abolished by either acetylsalicylic acid (ASA) or aprotonin and enhanced by captopril. The hypotensive action of kallikrein was only partially inhibited by ASA. It is proposed that both these pharmacological effects of kallikrein are mediated by bradykinin which in turn releases prostacyclin from the endothelium. However, in contrast to the thrombolytic effect of kallikrein which is totally mediated by prostacyclin the hypotensive action of kallikrein depends not only on prostacycylin but also on another endothelium-derived vasorelaxant, e.g. EDRF.

9

Properties of chemically oxidized kininogens.

75%

Niziołek M. , Kot M. , Pyka K. , Mak P. , Kozik A.

Acta Biochimica Polonica

|

2003

|

tom 50

|

nr 3

753-763

EN

Kininogens are multifunctional proteins involved in a variety of regulatory processes including the kinin-formation cascade, blood coagulation, fibrynolysis, inhibition of cysteine proteinases etc. A working hypothesis of this work was that the properties of kininogens may be altered by oxidation of their methionine residues by reactive oxygen species that are released at the inflammatory foci during phagocytosis of pathogen particles by recruited neutrophil cells. Two methionine-specific oxidizing reagents, N-chlorosuccinimide (NCS) and chloramine-T (CT), were used to oxidize the high molecular mass (HK) and low molecular mass (LK) forms of human kininogen. A nearly complete conversion of methionine residues to methionine sulfoxide residues in the modified proteins was determined by amino acid analysis. Production of kinins from oxidized kininogens by plasma and tissue kallikreins was significantly lower (by at least 70%) than that from native kininogens. This quenching effect on kinin release could primarily be assigned to the modification of the critical Met-361 residue adjacent to the internal kinin sequence in kininogen. However, virtually no kinin could be formed by human plasma kallikrein from NCS-modified HK. This observation suggests involvement of other structural effects detrimental for kinin production. Indeed, NCS-oxidized HK was unable to bind (pre)kallikrein, probably due to the modification of methionine and/or tryptophan residues at the region on the kininogen molecule responsible for the (pro)enzyme binding. Tests on papain inhibition by native and oxidized kininogens indicated that the inhibitory activity of kininogens against cysteine proteinases is essentially insensitive to oxidation.

10

Diagnosis of hereditary angioedema

75%

Kőhalmi K. V. , Cervenak L. , Farkas H.

Alergia Astma Immunologia - przegląd kliniczny

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2018

|

tom 23

|

nr 4

168-174

EN

Hereditary angioedema (HAE) is a rare disorder characterized by acute episodes of edema formation in the subcutis and/or the submucosa. The clinical picture of the disease resembles that of histamine-mediated angioedema, nevertheless bradykinin release is involved in the pathomechanism of HAE. The diagnosis of HAE can be established from the clinical manifestations, the family history, as well as the findings of complement and genetic tests. Currently, the six types of hereditary angioedema are distinguished: types I and II of hereditary angioedema with C1-inhibitor (C1-INH) deficiency (C1-INH-HAE) and the following types of hereditary angioedema with normal C1-INH levels: hereditary angioedema caused by a mutation in the Factor XII gene (FXII-HAE), the angiopoietin-1 gene (ANGPT1-HAE), and the plasminogen gene (PLG-HAE) – and hereditary angioedema of unknown origin (U-HAE). Current options for the laboratory diagnosis of angioedemas include means for identifying C1-INH-HAE, FXII-HAE, ANGPT1-HAE, PLG-HAE and acquired angioedema with C1-INH deficiency (C1-INH-AAE). No laboratory method is available currently for diagnosing the other types of angioedemas such as idiopathic histaminergic acquired angioedema (IH-AAE), idiopathic non-histaminergic acquired angioedema (InH-AAE), acquired angioedema related to angiotensin-converting enzyme inhibitor (ACEI-AAE), and U-HAE. These disease types can be identified only by indirect methods, i.e. by exploring medical and family history, observing the clinical manifestations and the therapeutic response, as well as by excluding the presence of C1-INH deficiency, FXII-HAE, ANGPT1-HAE, and PLG-HAE.

11

Properties of chemically oxidized kininogens

75%

Niziolek M. , Kot M. , Pyka K. , Mak P. , Kozik A.

Acta Biochimica Polonica

|

2003

|

tom 50

|

nr 3

EN

Kininogens are multifunctional proteins involved in a variety of regulatory processes including the kinin-formation cascade, blood coagulation, fibrynolysis, inhibition of cysteine proteinases etc. A working hypothesis of this work was that the properties of kininogens may be altered by oxidation of their methionine residues by reactive oxygen species that are released at the inflammatory foci during phagocytosis of pathogen particles by recruited neutrophil cells. Two methionine-specific oxidizing reagents, .-chlorosuccinimide (NCS) and chloramine-T (CT), were used to oxidize the high molecular mass (HK) and low molecular mass (LK) forms of human kininogen. A nearly complete conversion of methionine residues to methionine sulfoxide residues in the modified proteins was determined by amino acid analysis. Production of kinins from oxidized kininogens by plasma and tissue kallikreins was significantly lower (by at least 70%) than that from native kininogens. This quenching effect on kinin release could primarily be assigned to the modification of the critical Met-361 residue adjacent to the internal kinin sequence in kininogen. However, virtually no kinin could be formed by human plasma kallikrein from NCS-modified HK. This observation suggests involvement of other structural effects detrimental for kinin production. Indeed, NCS-oxidized HK was unable to bind (pre)kallikrein, probably due to the modification of methionine and/or tryptophan residues at the region on the kininogen molecule responsible for the (pro)enzyme binding. Tests on papain inhibition by native and oxidized kininogens indicated that the inhibitory activity of kininogens against cysteine proteinases is essentially insensitive to oxidation.

12

Influence of bradykinin and ACE inhibitors on selected biochemical markers of oxidative stress in rats with induced ischemia-reperfusion syndrome

63%

Krauss H. , Sosnowski P. , Grzymislawski M. , Kozlik J. , Jablecka A. , Balcer N. , Bednarek A.

Medycyna Weterynaryjna

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2007

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tom 63

|

nr 09

1052-1056

EN

Cessation of blood flow in tissues leads to depletion of energetic resources of cells, disturbances in the activity of enzymes of the oxidative chain and electrolyte disorders, as well as to the production of reactive oxygen species. A great deal of attention has been paid to those problems since they are responsible for most of the complications in the ischemia-reperfusion (I/R) syndrome. Understanding the antioxidative mechanisms involved in I/R syndrome provides us with the potential to correct at least some of the resulting disturbances. One of the potentially beneficial factors is insulin. This observation directed our attention to the insulin-like factors, kinins (especially bradykinin), the activation of which was detected in I/R syndrome. The effect of bradykinin is modified by concurrent administration of the specific antagonists of bradykinin receptors, B1 and B2. The aim of the current study was to assess the role of bradykinin. In the study, the employed agents included the angiotensin converting enzyme inhibitor, which prevents the degradation of endogenous kinins, and blockers of bradykinin receptors, which abolish the influence of kinins. We observed that after 4 hours of ischemia followed by reperfusion, levels of free radicals in tissues as well as levels of peroxides in plasma increased significantly. Administration of bradykinin, captopril or enalapril resulted in the decline of these free radical levels. The application of B2 receptor antagonist decreased the beneficial influence of bradykinin, whereas B1 receptor antagonist revealed no significant effect. Activities of antioxidative enzymes (superoxide dismutase, catalase, and glutathione peroxidase) were measured. After 4 hours of ischemia and consecutive steps of reperfusion, a statistically significant increase in their activities was observed when bradykinin or ACE inhibitors were administered. Application of B2 receptor blockers reduced the effect of bradykinin, whereas the effect of B1 receptor antagonists was minute.

13

Postconditioning effectively prevents trimethyltin induced neuronal damage in the rat brain

63%

Lalkovicova M. , Burda J. , Nemethova M. , Burda R. , Danielisova V.

Folia Biologica

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2016

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tom 64

|

nr 2

14

Potential role of bradykinin and its receptors in COVID-19

63%

Obtułowicz K. , Dubiela P. , Madaliński K. , Dyga W. , Obtułowicz P.

Alergia Astma Immunologia - przegląd kliniczny

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2021

|

tom 26

|

nr 2-3

46-53

PL

Bradykinina (BK) jest nonapeptydem należącym do rodziny kinin. Jest aktywnym mediatorem stanu zapalnego, który wywiera wiele różnych efektów poprzez swoje receptory B1 i B2 (B1R i B2R), jednak jej rola nie została do tej pory w pełni wyjaśniona. Wiadomo, że B1R i B2R oddziałują z białkiem konwertazy angiotensyny (ACE)-2, która działa jako receptor dla koronawirusa 2 (SARS-CoV-2), wywołującego chorobę COVID-19. Poprzez degradację BK do jego metabolitu desARG9-BK, ACE2 prowadzi do aktywacji B1R, co wyzwala uwalnianie cytokin pro- i przeciwzapalnych w odpowiedzi immunologicznej na patogeny. Z drugiej strony, ACE2 poprzez aktywację osi ANG(1-7)-MasR, stymuluje ekspresję B2R, która jest niezbędna dla prawidłowej funkcji śródbłonka. Kontrolowany wzrost uwalniania cytokin indukowany przez B1R podczas wnikania SARS-CoV-2 do komórek może być uznany za normalną odpowiedź immunologiczną zapobiegającą zakażeniu. Jeśli jednak mechanizmy regulacyjne zawiodą, wzrost uwalniania cytokin prozapalnych może prowadzić do progresji zakażenia, aktywacji śródbłonka i nasilenia objawów, w tym zajęcia narządów. Dostępne dane jednoznacznie sugerują, że BK i jego receptory są zaangażowane w patomechanizm COVID-19 i powiązane na drodze różnych mechanizmów sprzężenia zwrotnego z ACE2, ACE1, a także angiotensyną II (ANGII) i jej receptorami. Ponieważ ekspresja tych szlaków prawdopodobnie zmienia się dynamicznie w różnych stadiach COVID-19, należy opracować nowe opcje terapeutyczne ukierunkowane na te szlaki, ściśle monitorując ich aktywność.

EN

Bradykinin (BK) is a nonapeptide that belongs to the kinin family. It is an active inflammatory mediator that exerts multiple different effects via its B1 and B2 receptors (B1R and B2R); however, its role has not been fully elucidated so far. It is known that B1R and B2R interact with angiotensin-converting enzyme (ACE)-2 protein, which acts as a receptor for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that causes coronavirus disease 2019 (COVID-19). By degrading BK to its desARG9-BK metabolite, ACE2 leads to B1R activation, which triggers a release of pro- and anti-inflammatory cytokines in an immune response to infectious pathogens. On the other hand, ACE2 stimulates the expression of B2R by activating the ANG(1-7)–MasR axis which is essential for proper endothelial function. A controlled increase in B1R-mediated cytokine release during SARS-CoV-2 cell entry may be considered a normal immune response aiming to prevent infection. However, if regulatory mechanisms fail, the increase in proinflammatory cytokine release may lead to progression of infection, endothelial activation, and onset of symptoms, including organ involvement. Available data strongly suggest that BK and its receptors are involved in the pathomechanism of COVID-19 and linked by various feedback mechanisms to ACE2, ACE1, as well as angiotensin II (ANGII) and its receptors. As expression of these pathways is likely to change dynamically throughout different stages of COVID-19, novel treatment options that target these pathways along with close monitoring of their activity should be developed.

15

Intrarenal vasodilator systems: NO, prostaglandins and bradykinin. An integrative approach

63%

Sadowski J. , Badzynska B.

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tom 59

|

nr 9

105-119

16

In vitro studies of activation of phagocytic cells by bioactive peptides

63%

Stoika R. S. , Lutsik M. D. , Barska M. L. , Tsyrulnyk A. A. , Kashchak N. I.

Journal of Physiology and Pharmacology

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2002

|

tom 53

|

nr 4,1

EN

The effect of formyl chemotactic peptide (fCTP, fMet-Leu-Phe), ß-amyloid peptides (ß-AP, 1-42, 1-16 and 25-35), and bradykinin (BK) on functional activity of phagocytic cells has been investigated. Wheat germ agglutinin (WGA) was also used as a model membrane binding agent of polypeptide nature. Murine monocyte- macrophage cell line J774.2 and normal human blood polymorphonuclear (PMN) cells were used as target phagocytic cells. Their activity was quantitatively estimated by measuring phagocytosis of killed yeast cells. ß-AP (1-41) maximally stimulated phagocytosis at 0.1 µg/ml, BK - at 1.0 µg/ml, and fCTP - at 2.0 µg/ml. ß-AP (1-16) and ß-AP (25-35) were inactive in used test-systems. Phagocytosis-inducing activity of ß-AP (1-42) and BK reached maximal levels in 2 h and decreased after 4-6 h of incubation. Phagocytosis numbers were compared with the indicators of phagocytic cell activation, such as absorption of neutral red dye, glucose utilization, production of super-oxide anion (NBT-test) and nitrite accumulation (indicator of NO production). NBT-test, which may be related to the killing ability of phagocytic cells towards the ingested objects, was positive only in stimulated PMN leukocytes, while the nitrite accumulation was detected only in stimulated macrophages. Nitrite accumulation in macrophages was markedly induced by lipopolysaccharide and to a lower extent by 0.5 µg/ml ß-AP (1-42). In high dose (5.0 µg/ml) ß-AP suppressed nitrite accumulation in macrophages stimulated by lipopolysaccharide. Other studied peptides were inactive in inducing nitrite accumulation. Transforming growth factor type ß suppressed phagocytic activity of PMN cells activated by ß-AP or WGA. The anti-inflammatory drugs (indomethacin and L-lysine aescinate) inhibited ß-AP (1- 42)-induced phagocytosis. The interrelations between the regulatory pathways of BK, ß-AP and fCTP are discussed.

17

Is bradykinin [BK] a physiological vasodilator in the gut?

63%

Jacobson E. D. , Berguer R. , Higgins A. , Stewart J. M.

|

nr 4

18

Bradykinin in ischemia-reperfusion injury of the rat lung

51%

Nowak K. , Weih S. , Post S. , Gebhard M. M. , Hohenberger P.

Journal of Physiology and Pharmacology. Supplement

|

2007

|

tom 58

|

nr 5

19

Human endothelial lectin-like oxLDL receptor-1 (LOX-1) expression is not associated with impairment of endothelium-dependent vasoreactivity in conduit vessels

51%

Wetterau E. , Stecher S.-S. , Wolff B. , Khouri S. , Staudt A. , Felix S. B. , Landsberger M.

Journal of Physiology and Pharmacology

|

2013

|

tom 64

|

nr 4

20

Long-term feeding with bioactive tripeptides in aged hypertensive and normotensive rats: special focus on blood pressure and bradykinin-induced vascular reactivity

51%

Siltari A. , Roivanen J. , Korpela R. , Vapaatalo H.

Journal of Physiology and Pharmacology

|

2017

|

tom 68

|

nr 3