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1

Kallikrein-thrombolytic and hypotensive action in cats - preliminary results

100%
Swies J., Grodzinska L., Slawinski M., Gryglewski R. J.
Acta Physiologica Polonica
|
1990
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tom 41
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nr 1-3
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.
2

Properties of chemically oxidized kininogens

100%
Niziolek M., Kot M., Pyka K., Mak P., Kozik A.
Acta Biochimica Polonica
|
2003
|
tom 50
|
nr 3
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.
3
Content available remote

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

84%
Sadowski J., Badzynska B.
Journal of Physiology and Pharmacology. Supplement
|
2008
|
tom 59
|
nr 9
105-119
4

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

84%
Krauss H., Sosnowski P., Grzymislawski M., Kozlik J., Jablecka A., Balcer N., Bednarek A.
Medycyna Weterynaryjna
|
2007
|
tom 63
|
nr 09
1052-1056
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.
5

Postconditioning effectively prevents trimethyltin induced neuronal damage in the rat brain

84%
Lalkovicova M., Burda J., Nemethova M., Burda R., Danielisova V.
Folia Biologica
|
2016
|
tom 64
|
nr 2
6
Content available remote

In vitro studies of activation of phagocytic cells by bioactive peptides

84%
Stoika R. S., Lutsik M. D., Barska M. L., Tsyrulnyk A. A., Kashchak N. I.
Journal of Physiology and Pharmacology
|
2002
|
tom 53
|
nr 4,1
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.
7
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Content available

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

84%
Jacobson E. D., Berguer R., Higgins A., Stewart J. M.
Journal of Physiology and Pharmacology
|
1993
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tom 44
|
nr 4
8
Content available remote

Bradykinin in ischemia-reperfusion injury of the rat lung

67%
Nowak K., Weih S., Post S., Gebhard M. M., Hohenberger P.
Journal of Physiology and Pharmacology. Supplement
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2007
|
tom 58
|
nr 5
9
Content available remote

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

67%
Siltari A., Roivanen J., Korpela R., Vapaatalo H.
Journal of Physiology and Pharmacology
|
2017
|
tom 68
|
nr 3
10
Content available remote

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

67%
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
11
Content available remote

Paradoxical augmentation of bradykinin-induced vasodilatation by xanthine-xanthine oxidase-derived free radicals in isolated guinea pig heart

67%
Olszanecki R., Kozlovski V. I., Chlopicki S., Gryglewski R. J.
Journal of Physiology and Pharmacology
|
2002
|
tom 53
|
nr 4,1
Increased generation of reactive oxygen species contribute to endothelial dysfunction in atherosclerosis, hypertension and heart failure. Recently, it was suggested that bursts of superoxide anions may inactivate endothelial surface-bound enzymes such as angiotensin converting enzyme (ACE). Here, we tested effects of xanthine/xanthine oxidase-derived superoxide anions on vascular responses and ACE activity in the isolated guinea pig heart. We analysed effects of intracoronary infusion of low concentration of xanthine oxidase (10 mU/ml) in the presence of xanthine (0,5 mM) (X/XO) on bradykinin, other endothelium-dependent and independent vasodilators (acetylcholine, ADP, SNAP), as well as vasoconstrictor responses to angiotensin I and angiotensin II. Surprisingly, X/XO significantly augmented coronary response to bradykinin without an effect on responses to ADP, acetylcholine, SNAP, angiotensin I and angiotensin II. In contrast, inhibition of ACE by perindoprilate (100 nM) resulted in augmentation of bradykinin-induced vasodilatation as well as diminution of angiotensin I-evoked vasoconstriction without an influence on other responses. In summary, in the isolated guinea pig heart, X/XO-derived free radicals selectively augmented coronary vasodilator response to bradykinin, which cannot be explained by X/XO- induced derangement of ACE. The mechanism of this paradoxical phenomenon, which might represent a defensive response of the coronary circulation to oxidative stress requires further investigations.
12

NANC transmission in intestines and its pharmacological modulation

59%
Bauer V.
Acta Neurobiologiae Experimentalis
|
1993
|
tom 53
|
nr 1
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