A nonapeptide messenger that is enzymatically produced from KALLIDIN in the blood where it is a potent but short-lived agent of arteriolar dilation and increased capillary permeability. Bradykinin is also released from MAST CELLS during asthma attacks, from gut walls as a gastrointestinal vasodilator, from damaged tissues as a pain signal, and may be a neurotransmitter.
Cell surface receptors that bind BRADYKININ and related KININS with high affinity and trigger intracellular changes which influence the behavior of cells. The identified receptor types (B-1 and B-2, or BK-1 and BK-2) recognize endogenous KALLIDIN; t-kinins; and certain bradykinin fragments as well as bradykinin itself.
A constitutively expressed subtype of bradykinin receptor that may play a role in the acute phase of the inflammatory and pain response. It has high specificity for intact forms of BRADYKININ and KALLIDIN. The receptor is coupled to G-PROTEIN, GQ-G11 ALPHA FAMILY and G-PROTEIN, GI-GO ALPHA FAMILY signaling proteins.
A subtype of BRADYKININ RECEPTOR that is induced in response to INFLAMMATION. It may play a role in chronic inflammation and has a high specificity for KININS lacking the C-terminal ARGININE such as des-Arg(10)-kallidin and des-Arg(9)-bradykinin. The receptor is coupled to G-PROTEIN, GQ-G11 ALPHA FAMILY and G-PROTEIN, GI-GO ALPHA FAMILY signaling proteins.
A decapeptide bradykinin homolog cleaved from kininogen by kallikreins. It is a smooth-muscle stimulant and hypotensive agent that acts by vasodilatation.
A generic term used to describe a group of polypeptides with related chemical structures and pharmacological properties that are widely distributed in nature. These peptides are AUTACOIDS that act locally to produce pain, vasodilatation, increased vascular permeability, and the synthesis of prostaglandins. Thus, they comprise a subset of the large number of mediators that contribute to the inflammatory response. (From Goodman and Gilman's The Pharmacologic Basis of Therapeutics, 8th ed, p588)
A system of metabolic interactions by products produced in the distal nephron of the KIDNEY. These products include KALLIKREIN; KININS; KININASE I; KININASE II; and ENKEPHALINASE. This system participates in the control of renal functions. It interacts with the RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM to regulate BLOOD PRESSURE, generation of PROSTAGLANDINS, release of VASOPRESSINS, and WATER-ELECTROLYTE BALANCE.
A class of drugs whose main indications are the treatment of hypertension and heart failure. They exert their hemodynamic effect mainly by inhibiting the renin-angiotensin system. They also modulate sympathetic nervous system activity and increase prostaglandin synthesis. They cause mainly vasodilation and mild natriuresis without affecting heart rate and contractility.
Endogenous peptides present in most body fluids. Certain enzymes convert them to active KININS which are involved in inflammation, blood clotting, complement reactions, etc. Kininogens belong to the cystatin superfamily. They are cysteine proteinase inhibitors. HIGH-MOLECULAR-WEIGHT KININOGEN; (HMWK); is split by plasma kallikrein to produce BRADYKININ. LOW-MOLECULAR-WEIGHT KININOGEN; (LMWK); is split by tissue kallikrein to produce KALLIDIN.
Cell surface receptors that bind signalling molecules released by neurons and convert these signals into intracellular changes influencing the behavior of cells. Neurotransmitter is used here in its most general sense, including not only messengers that act to regulate ion channels, but also those which act on second messenger systems and those which may act at a distance from their release sites. Included are receptors for neuromodulators, neuroregulators, neuromediators, and neurohumors, whether or not located at synapses.
A non-steroidal anti-inflammatory agent (NSAID) that inhibits the enzyme cyclooxygenase necessary for the formation of prostaglandins and other autacoids. It also inhibits the motility of polymorphonuclear leukocytes.
A metallocarboxypeptidase that removes C-terminal basic amino acid from peptides and proteins, with preference shown for lysine over arginine. It is a plasma zinc enzyme that inactivates bradykinin and anaphylatoxins.
Proteolytic enzymes from the serine endopeptidase family found in normal blood and urine. Specifically, Kallikreins are potent vasodilators and hypotensives and increase vascular permeability and affect smooth muscle. They act as infertility agents in men. Three forms are recognized, PLASMA KALLIKREIN (EC 3.4.21.34), TISSUE KALLIKREIN (EC 3.4.21.35), and PROSTATE-SPECIFIC ANTIGEN (EC 3.4.21.77).
A potent and specific inhibitor of PEPTIDYL-DIPEPTIDASE A. It blocks the conversion of ANGIOTENSIN I to ANGIOTENSIN II, a vasoconstrictor and important regulator of arterial blood pressure. Captopril acts to suppress the RENIN-ANGIOTENSIN SYSTEM and inhibits pressure responses to exogenous angiotensin.
The physiological widening of BLOOD VESSELS by relaxing the underlying VASCULAR SMOOTH MUSCLE.
A free radical gas produced endogenously by a variety of mammalian cells, synthesized from ARGININE by NITRIC OXIDE SYNTHASE. Nitric oxide is one of the ENDOTHELIUM-DEPENDENT RELAXING FACTORS released by the vascular endothelium and mediates VASODILATION. It also inhibits platelet aggregation, induces disaggregation of aggregated platelets, and inhibits platelet adhesion to the vascular endothelium. Nitric oxide activates cytosolic GUANYLATE CYCLASE and thus elevates intracellular levels of CYCLIC GMP.
A peptidyl-dipeptidase that catalyzes the release of a C-terminal dipeptide, -Xaa-*-Xbb-Xcc, when neither Xaa nor Xbb is Pro. It is a Cl(-)-dependent, zinc glycoprotein that is generally membrane-bound and active at neutral pH. It may also have endopeptidase activity on some substrates. (From Enzyme Nomenclature, 1992) EC 3.4.15.1.
The active metabolite of ENALAPRIL and a potent intravenously administered angiotensin-converting enzyme inhibitor. It is an effective agent for the treatment of essential hypertension and has beneficial hemodynamic effects in heart failure. The drug produces renal vasodilation with an increase in sodium excretion.
Single pavement layer of cells which line the luminal surface of the entire vascular system and regulate the transport of macromolecules and blood components.
An amine derived by enzymatic decarboxylation of HISTIDINE. It is a powerful stimulant of gastric secretion, a constrictor of bronchial smooth muscle, a vasodilator, and also a centrally acting neurotransmitter.
The relationship between the dose of an administered drug and the response of the organism to the drug.
A long-acting angiotensin-converting enzyme inhibitor. It is a prodrug that is transformed in the liver to its active metabolite ramiprilat.
Drugs used to cause dilation of the blood vessels.
The property of blood capillary ENDOTHELIUM that allows for the selective exchange of substances between the blood and surrounding tissues and through membranous barriers such as the BLOOD-AIR BARRIER; BLOOD-AQUEOUS BARRIER; BLOOD-BRAIN BARRIER; BLOOD-NERVE BARRIER; BLOOD-RETINAL BARRIER; and BLOOD-TESTIS BARRIER. Small lipid-soluble molecules such as carbon dioxide and oxygen move freely by diffusion. Water and water-soluble molecules cannot pass through the endothelial walls and are dependent on microscopic pores. These pores show narrow areas (TIGHT JUNCTIONS) which may limit large molecule movement.
A group of compounds derived from unsaturated 20-carbon fatty acids, primarily arachidonic acid, via the cyclooxygenase pathway. They are extremely potent mediators of a diverse group of physiological processes.
A decapeptide that is cleaved from precursor angiotensinogen by RENIN. Angiotensin I has limited biological activity. It is converted to angiotensin II, a potent vasoconstrictor, after the removal of two amino acids at the C-terminal by ANGIOTENSIN CONVERTING ENZYME.
An eleven-amino acid neurotransmitter that appears in both the central and peripheral nervous systems. It is involved in transmission of PAIN, causes rapid contractions of the gastrointestinal smooth muscle, and modulates inflammatory and immune responses.
A potent inhibitor of membrane metalloendopeptidase (ENKEPHALINASE). Thiorphan potentiates morphine-induced ANALGESIA and attenuates naloxone-precipitated withdrawal symptoms.
A non-selective inhibitor of nitric oxide synthase. It has been used experimentally to induce hypertension.
A powerful vasodilator used in emergencies to lower blood pressure or to improve cardiac function. It is also an indicator for free sulfhydryl groups in proteins.
The veins and arteries of the HEART.
A basic element found in nearly all organized tissues. It is a member of the alkaline earth family of metals with the atomic symbol Ca, atomic number 20, and atomic weight 40. Calcium is the most abundant mineral in the body and combines with phosphorus to form calcium phosphate in the bones and teeth. It is essential for the normal functioning of nerves and muscles and plays a role in blood coagulation (as factor IV) and in many enzymatic processes.
A neurotransmitter found at neuromuscular junctions, autonomic ganglia, parasympathetic effector junctions, a subset of sympathetic effector junctions, and at many sites in the central nervous system.
An inhibitor of nitric oxide synthetase which has been shown to prevent glutamate toxicity. Nitroarginine has been experimentally tested for its ability to prevent ammonia toxicity and ammonia-induced alterations in brain energy and ammonia metabolites. (Neurochem Res 1995:200(4):451-6)
PRESSURE of the BLOOD on the ARTERIES and other BLOOD VESSELS.
An octapeptide that is a potent but labile vasoconstrictor. It is produced from angiotensin I after the removal of two amino acids at the C-terminal by ANGIOTENSIN CONVERTING ENZYME. The amino acid in position 5 varies in different species. To block VASOCONSTRICTION and HYPERTENSION effect of angiotensin II, patients are often treated with ACE INHIBITORS or with ANGIOTENSIN II TYPE 1 RECEPTOR BLOCKERS.
Endogenously-synthesized compounds that influence biological processes not otherwise classified under ENZYMES; HORMONES or HORMONE ANTAGONISTS.
A common name used for the genus Cavia. The most common species is Cavia porcellus which is the domesticated guinea pig used for pets and biomedical research.
A plasma protein, molecular weight of 110 kD, that normally exists in plasma in a 1:1 complex with PREKALLIKREIN. HMWK is split by plasma kallikrein to produce BRADYKININ. The complex is a cofactor in the activation of coagulation factor XII. The product of this reaction, XIIa, in turn activates prekallikrein to KALLIKREINS. (From Stedman, 26th ed)
A prostaglandin that is a powerful vasodilator and inhibits platelet aggregation. It is biosynthesized enzymatically from PROSTAGLANDIN ENDOPEROXIDES in human vascular tissue. The sodium salt has been also used to treat primary pulmonary hypertension (HYPERTENSION, PULMONARY).
Compounds or agents that combine with cyclooxygenase (PROSTAGLANDIN-ENDOPEROXIDE SYNTHASES) and thereby prevent its substrate-enzyme combination with arachidonic acid and the formation of eicosanoids, prostaglandins, and thromboxanes.
Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.
Abnormal fluid accumulation in TISSUES or body cavities. Most cases of edema are present under the SKIN in SUBCUTANEOUS TISSUE.
Unstriated and unstriped muscle, one of the muscles of the internal organs, blood vessels, hair follicles, etc. Contractile elements are elongated, usually spindle-shaped cells with centrally located nuclei. Smooth muscle fibers are bound together into sheets or bundles by reticular fibers and frequently elastic nets are also abundant. (From Stedman, 25th ed)
An alkylamide found in CAPSICUM that acts at TRPV CATION CHANNELS.
The domestic dog, Canis familiaris, comprising about 400 breeds, of the carnivore family CANIDAE. They are worldwide in distribution and live in association with people. (Walker's Mammals of the World, 5th ed, p1065)
The cartilaginous and membranous tube descending from the larynx and branching into the right and left main bronchi.
The most common and most biologically active of the mammalian prostaglandins. It exhibits most biological activities characteristic of prostaglandins and has been used extensively as an oxytocic agent. The compound also displays a protective effect on the intestinal mucosa.
(11 alpha,13E,15S)-11,15-Dihydroxy-9-oxoprost-13-en-1-oic acid (PGE(1)); (5Z,11 alpha,13E,15S)-11,15-dihydroxy-9-oxoprosta-5,13-dien-1-oic acid (PGE(2)); and (5Z,11 alpha,13E,15S,17Z)-11,15-dihydroxy-9-oxoprosta-5,13,17-trien-1-oic acid (PGE(3)). Three of the six naturally occurring prostaglandins. They are considered primary in that no one is derived from another in living organisms. Originally isolated from sheep seminal fluid and vesicles, they are found in many organs and tissues and play a major role in mediating various physiological activities.
Phosphoric acid esters of inositol. They include mono- and polyphosphoric acid esters, with the exception of inositol hexaphosphate which is PHYTIC ACID.
An NADPH-dependent enzyme that catalyzes the conversion of L-ARGININE and OXYGEN to produce CITRULLINE and NITRIC OXIDE.
A group of ISOQUINOLINES in which the nitrogen containing ring is protonated. They derive from the non-enzymatic Pictet-Spengler condensation of CATECHOLAMINES with ALDEHYDES.
Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction.
A strain of albino rat used widely for experimental purposes because of its calmness and ease of handling. It was developed by the Sprague-Dawley Animal Company.
Delivery of drugs into an artery.
Enzyme that is a major constituent of kidney brush-border membranes and is also present to a lesser degree in the brain and other tissues. It preferentially catalyzes cleavage at the amino group of hydrophobic residues of the B-chain of insulin as well as opioid peptides and other biologically active peptides. The enzyme is inhibited primarily by EDTA, phosphoramidon, and thiorphan and is reactivated by zinc. Neprilysin is identical to common acute lymphoblastic leukemia antigen (CALLA Antigen), an important marker in the diagnosis of human acute lymphocytic leukemia. There is no relationship with CALLA PLANT.
A strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.
Rapidly decreasing response to a drug or physiologically active agent after administration of a few doses. In immunology, it is the rapid immunization against the effect of toxic doses of an extract or serum by previous injection of small doses. (Dorland, 28th ed)
The action of a drug in promoting or enhancing the effectiveness of another drug.
The species Oryctolagus cuniculus, in the family Leporidae, order LAGOMORPHA. Rabbits are born in burrows, furless, and with eyes and ears closed. In contrast with HARES, rabbits have 22 chromosome pairs.
An essential amino acid that is physiologically active in the L-form.
A family of trypsin-like SERINE ENDOPEPTIDASES that are expressed in a variety of cell types including human prostate epithelial cells. They are formed from tissue prokallikrein by action with TRYPSIN. They are highly similar to PROSTATE-SPECIFIC ANTIGEN.
Any of various animals that constitute the family Suidae and comprise stout-bodied, short-legged omnivorous mammals with thick skin, usually covered with coarse bristles, a rather long mobile snout, and small tail. Included are the genera Babyrousa, Phacochoerus (wart hogs), and Sus, the latter containing the domestic pig (see SUS SCROFA).

Expression of both P1 and P2 purine receptor genes by human articular chondrocytes and profile of ligand-mediated prostaglandin E2 release. (1/3087)

OBJECTIVE: To assess the expression and function of purine receptors in articular chondrocytes. METHODS: Reverse transcriptase-polymerase chain reaction (RT-PCR) was used to screen human chondrocyte RNA for expression of P1 and P2 purine receptor subtypes. Purine-stimulated prostaglandin E2 (PGE2) release from chondrocytes, untreated or treated with recombinant human interleukin-1alpha (rHuIL-1alpha), was assessed by radioimmunoassay. RESULTS: RT-PCR demonstrated that human articular chondrocytes transcribe messenger RNA for the P1 receptor subtypes A2a and A2b and the P2 receptor subtype P2Y2, but not for the P1 receptor subtypes A1 and A3. The P1 receptor agonists adenosine and 5'-N-ethylcarboxamidoadenosine did not change PGE2 release from chondrocytes. The P2Y2 agonists ATP and UTP stimulated a small release of PGE2 that was potentiated after pretreatment with rHuIL-1alpha. PGE2 release in response to ATP and UTP cotreatment was not additive, but release in response to coaddition of ATP and bradykinin (BK) or UTP and BK was additive, consistent with ATP and UTP competition for the same receptor site. The potentiation of PGE2 release in response to ATP and UTP after rHuIL-1alpha pretreatment was mimicked by phorbol myristate acetate. CONCLUSION: Human chondrocytes express both P1 and P2 purine receptor subtypes. The function of the P1 receptor subtype is not yet known, but stimulation of the P2Y2 receptor increases IL-1-mediated PGE2 release.  (+info)

Endothelial function in Marfan syndrome: selective impairment of flow-mediated vasodilation. (2/3087)

BACKGROUND: The cardiovascular complications of Marfan syndrome arise due to alterations in the structural and functional properties of fibrillin, a constituent of vascular connective tissues. Fibrillin-containing microfibrils are closely associated with arterial endothelial cells, indicating a possible functional role for fibrillin in the endothelium. Plasma concentrations of endothelial cell products are elevated in Marfan subjects, which indirectly indicates endothelial dysfunction. This study directly assessed flow- and agonist-mediated endothelium-dependent brachial artery reactivity in Marfan subjects. METHODS AND RESULTS: In 20 Marfan and 20 control subjects, brachial artery diameter, blood flow, and blood pressure were measured by ultrasonic wall tracking, Doppler ultrasound, and photoplethysmography, respectively. Measurements were taken during hand hyperemia (a stimulus for endothelium-derived nitric oxide [NO] release in the upstream brachial artery) and after sublingual administration of the endothelium-independent vasodilator nitroglycerin. In 9 Marfan and 6 control subjects, the above parameters were also assessed during intra-arterial infusions of acetylcholine and bradykinin (agonists that stimulate NO production) and NG-monomethyl-L-arginine (L-NMMA, an inhibitor of NO production). Flow-mediated responses differed markedly between Marfan and control subjects (-1.6+/-3.5% versus 6. 50+/-4.1%, respectively; P<0.0001), whereas nitroglycerin produced similar vasodilation (14.2+/-5.7% versus 15.2+/-7.8%; P=NS). Agonist-induced vasodilation to incremental intra-arterial infusions of acetylcholine and bradykinin were not significantly different between Marfan and control subjects, and intra-arterial L-NMMA produced similar reductions in brachial artery diameter in both groups. CONCLUSIONS: These data demonstrate impaired flow-mediated but preserved agonist-mediated endothelium-dependent vasodilation in Marfan subjects and suggest preservation of basal NO release. Selective loss of flow-mediated dilation suggests a role for fibrillin in endothelial cell mechanotransduction.  (+info)

Bradykinin promotes ischemic norepinephrine release in guinea pig and human hearts. (3/3087)

We previously reported that bradykinin (BK; 1-1000 nM) facilitates norepinephrine (NE) release from cardiac sympathetic nerves. Because BK production increases in myocardial ischemia, endogenous BK could foster NE release and associated arrhythmias. We tested this hypothesis in guinea pig and human myocardial ischemia models. BK administration (100 nM) markedly enhanced exocytotic and carrier-mediated NE overflow from guinea pig hearts subjected to 10- and 20-min ischemia/reperfusion, respectively. Ventricular fibrillation invariably occurred after 20-min global ischemia; BK prolonged its duration 3-fold. The BK B2 receptor antagonist HOE140 (30 nM) blocked the effects of BK, whereas the B1 receptor antagonist des-Arg9-Leu8-BK (1 microM; i.e., 2.5 x pA2) did not. When serine proteinase inhibitors (500 KIU/ml aprotinin and 100 microg/ml soybean trypsin inhibitor) were used to prevent the formation of endogenous BK, NE overflow and reperfusion arrhythmias were diminished. In contrast, when kininase I and II inhibitors (DL-2-mercaptomethyl-3-guanidinoethylthiopropanoic acid and enalaprilat, each 1 microM) were used to prevent the degradation of endogenous BK, NE overflow and reperfusion arrhythmias were enhanced. B2 receptor blockade abolished these effects but was ineffective if kininases were not inhibited. B2 receptor stimulation, by either exogenous or endogenous BK, also markedly enhanced carrier-mediated NE release in the human myocardial ischemia model; conversely, inhibition of BK biosynthesis diminished ischemic NE release. Because atherosclerotic heart disease impairs endothelial BK production, in myocardial ischemia BK could accumulate at sympathetic nerve endings, thus augmenting exocytotic and carrier-mediated NE release and favoring coronary vasoconstriction and arrhythmias.  (+info)

Mechanisms of prostaglandin E2 release by intact cells expressing cyclooxygenase-2: evidence for a 'two-component' model. (4/3087)

Prostaglandin (PG) release in cells expressing constitutive cyclooxygenase-1 is known to be regulated by liberation of arachidonic acid by phospholipase A2 followed by metabolism by cyclooxygenase. However, the relative contribution of phospholipase A2 to the release of PGs in cells expressing cyclooxygenase-2 is not clear. We addressed this question by using radioimmunoassay to measure PGE2 release by human cells (A549) induced to express cyclooxygenase-2 (measured by Western blot analysis) by interleukin-1beta. Cells were either unstimulated or stimulated with agents known to activate phospholipase A2 (bradykinin, Des-Arg10-kallidin, or the calcium ionophore A23187) or treated with exogenous arachidonic acid. When cells were treated to express cyclooxygenase-2, the levels of PGE2 released over 15 min were undetectable; however, in the same cells stimulated with bradykinin, A23187, or arachidonic acid, large amounts of prostanoid were produced. Using selective inhibitors/antagonists, we found that the effects of bradykinin were mediated by B2 receptor activation and that prostanoid release was due to cyclooxygenase-2, and not cyclooxygenase-1, activity. In addition, we show that the release of PGE2 stimulated by either bradykinin, A23187, or arachidonic acid was inhibited by the phospholipase A2 inhibitor arachidonate trifluoromethyl ketone. Hence, we have demonstrated that PGE2 is released by two components: induction of cyclooxygenase-2 and supply of substrate, probably via activation of phospholipase A2. This is illustrated in A549 cells by a clear synergy between the cytokine interleukin-1beta and the kinin bradykinin.  (+info)

Blocking angiotensin II ameliorates proteinuria and glomerular lesions in progressive mesangioproliferative glomerulonephritis. (5/3087)

BACKGROUND: The renin-angiotensin system is thought to be involved in the progression of glomerulonephritis (GN) into end-stage renal failure (ESRF) because of the observed renoprotective effects of angiotensin-converting enzyme inhibitors (ACEIs). However, ACEIs have pharmacological effects other than ACE inhibition that may help lower blood pressure and preserve glomerular structure. We previously reported a new animal model of progressive glomerulosclerosis induced by a single intravenous injection of an anti-Thy-1 monoclonal antibody, MoAb 1-22-3, in uninephrectomized rats. Using this new model of progressive GN, we examined the hypothesis that ACEIs prevent the progression to ESRF by modulating the effects of angiotensin II (Ang II) on the production of transforming growth factor-beta (TGF-beta) and extracellular matrix components. METHODS: We studied the effect of an ACEI (cilazapril) and an Ang II type 1 receptor antagonist (candesartan) on the clinical features and morphological lesions in the rat model previously reported. After 10 weeks of treatment with equihypotensive doses of cilazapril, cilazapril plus Hoe 140 (a bradykinin receptor B2 antagonist), candesartan, and hydralazine, we examined systolic blood pressure, urinary protein excretion, creatinine clearance, the glomerulosclerosis index, and the tubulointerstitial lesion index. We performed a semiquantitative evaluation of glomerular immunostaining for TGF-beta and collagen types I and III by immunofluorescence study and of these cortical mRNA levels by Northern blot analysis. RESULTS: Untreated rats developed massive proteinuria, renal dysfunction, and severe glomerular and tubulointerstitial injury, whereas uninephrectomized control rats did not. There was a significant increase in the levels of glomerular protein and cortical mRNA for TGF-beta and collagen types I and III in untreated rats. Cilazapril and candesartan prevented massive proteinuria, increased creatinine clearance, and ameliorated glomerular and tubulointerstitial injury. These drugs also reduced levels of glomerular protein and cortical mRNA for TGF-beta and collagen types I and III. Hoe 140 failed to blunt the renoprotective effect of cilazapril. Hydralazine did not exhibit a renoprotective effect. CONCLUSION: These results indicate that ACEIs prevent the progression to ESRF by modulating the effects of Ang II via Ang II type 1 receptor on the production of TGF-beta and collagen types I and III, as well as on intrarenal hemodynamics, but not by either increasing bradykinin activity or reducing blood pressure in this rat model of mesangial proliferative GN.  (+info)

Activation of the kallikrein-kinin system in hemodialysis: role of membrane electronegativity, blood dilution, and pH. (6/3087)

BACKGROUND: The kallikrein-kinin system activation by contact with a negatively charged surface has been promulgated to be responsible for hypersensitivity reactions. However, to explain the low frequency and heterogeneity of hypersensitivity reactions, we hypothesized that not only the electronegativity of the membrane, but also other physicochemical parameters could influence the activation of the contact phase system of plasma assessed by the measurement of kallikrein activity and bradykinin concentration. METHODS: Plasma kallikrein activity using chromogenic substrate (S2302) and plasma bradykinin concentration (enzyme immuno assay) were measured during the perfusion of human plasma (2.5 ml/min) through minidialyzers mounted with six different membranes [polyacrylonitrile (PAN) from Asahi (PANDX) and from Hospal (AN69), polymethylmethacrylate (PMMA) from Toray, cellulose triacetate (CT) from Baxter, cuprophane (CUP) from Akzo and polysulfone (PS) from Fresenius]. RESULTS: A direct relationship was shown between the electronegativity of the membrane assessed by its zeta potential and the activation of plasma during the first five minutes of plasma circulation. With the AN69 membrane, the detection of a kallikrein activity in diluted plasma but not in undiluted samples confirmed the importance of a protease-antiprotease imbalance leading to bradykinin release during the first five minutes of dialysis. With PAN membranes, the use of citrated versus heparinized plasma and the use of various rinsing solutions clearly show a dramatic effect of pH on the kallikrein activity and the bradykinin concentration measured in plasma. Finally, increasing the zeta potential of the membrane leads to a significant increase of plasma kallikrein activity and bradykinin concentration. CONCLUSIONS: Our in vitro experimental approach evidences the importance of the control of these physicochemical factors to decrease the activation of the contact system.  (+info)

Cytokine-mediated inflammatory hyperalgesia limited by interleukin-4. (7/3087)

1. The effect of IL-4 on responses to intraplantar (i.pl.) carrageenin, bradykinin, TNFalpha, IL-1beta, IL-8 and PGE2 was investigated in a model of mechanical hyperalgesia in rats. Also, the cellular source of the IL-4 was investigated. 2. IL-4, 30 min before the stimulus, inhibited responses to carrageenin, bradykinin, and TNFalpha, but not responses to IL-1beta, IL-8 and PGE2. 3. IL-4, 2 h before the injection of IL-1beta, did not affect the response to IL-1beta, whereas IL-4, 12 or 12+2 h before the IL-1beta, inhibited the hyperalgesia (-30%, -74%, respectively). 4. In murine peritoneal macrophages, murine IL-4 for 2 h before stimulation with LPS, inhibited (-40%) the production of IL-1beta but not PGE2. Murine IL-4 (for 16 h before stimulation with LPS) inhibited LPS-stimulated PGE2 but not IL-1beta. 5. Anti-murine IL-4 antibodies potentiated responses to carrageenin, bradykinin and TNFalpha, but not IL-1beta and IL-8, as well as responses to bradykinin in athymic rats but not in rats depleted of mast cells with compound 40/80. 6. These data suggest that IL-4 released by mast cells limits inflammatory hyperalgesia. During the early phase of the inflammatory response the mode of action of the IL-4 appears to be inhibition of the production TNFalpha, IL-1beta and IL-8. In the later phase of the response, in addition to inhibiting the production of pro-inflammatory cytokines, IL-4 also may inhibit the release of PGs.  (+info)

Nitric oxide limits the eicosanoid-dependent bronchoconstriction and hypotension induced by endothelin-1 in the guinea-pig. (8/3087)

1. This study attempts to investigate if endogenous nitric oxide (NO) can modulate the eicosanoid-releasing properties of intravenously administered endothelin-1 (ET-1) in the pulmonary and circulatory systems in the guinea-pig. 2. The nitric oxide synthase blocker N(omega)-nitro-L-arginine methyl ester (L-NAME; 300 microM; 30 min infusion) potentiated, in an L-arginine sensitive fashion, the release of thromboxane A2 (TxA2) stimulated by ET-1, the selective ET(B) receptor agonist IRL 1620 (Suc-[Glu9,Ala11,15]-ET-1(8-21)) or bradykinin (BK) (5, 50 and 50 nM, respectively, 3 min infusion) in guinea-pig isolated and perfused lungs. 3. In anaesthetized and ventilated guinea-pigs intravenous injection of ET-1 (0.1-1.0 nmol kg(-1)), IRL 1620 (0.2-1.6 nmol kg(-1)), BK (1.0-10.0 nmol kg(-1)) or U 46619 (0.2-5.7 nmol kg(-1)) each induced dose-dependent increases in pulmonary insufflation pressure (PIP). Pretreatment with L-NAME (5 mg kg(-1)) did not change basal PIP, but increased, in L-arginine sensitive manner, the magnitude of the PIP increases (in both amplitude and duration) triggered by each of the peptides (at 0.25, 0.4 and 1.0 nmol kg(-1), respectively), without modifying bronchoconstriction caused by U 46619 (0.57 nmol kg(-1)). 4. The increases in PIP induced by ET-1, IRL 1620 (0.25 and 0.4 nmol kg(-1), respectively) or U 46619 (0.57 nmol kg(-1)) were accompanied by rapid and transient increases of mean arterial blood pressure (MAP). Pretreatment with L-NAME (5 mg kg(-1); i.v. raised basal MAP persistently and, under this condition, subsequent administration of ET-1 or IRL 1620, but not of U-46619, induced hypotensive responses which were prevented by pretreatment with the cyclo-oxygenase inhibitor indomethacin. 5. Thus, endogenous NO appears to modulate ET-1-induced bronchoconstriction and pressor effects in the guinea-pig by limiting the peptide's ability to induce, possibly via ET(B) receptors, the release of TxA2 in the lungs and of vasodilatory prostanoids in the systemic circulation. Furthermore, it would seem that these eicosanoid-dependent actions of ET-1 in the pulmonary system and on systemic arterial resistance in this species are physiologically dissociated.  (+info)

In this study we evaluated the mechanisms underlying s.c. and spinal intrathecal (i.t.) nicotine inhibition of bradykinin-induced plasma extravasation in the knee joint of the rat (J. Pharmacol. Exp. Ther. 262: 889-895, 1992; ibid., 264: 839-844, 1993). The dose-response curve for the inhibitory action of s.c. nicotine on bradykinin-induced plasma extravasation was attenuated by adrenal medullectomy and by intra-articular perfusion of ICI-118,551 (a beta-2 adrenoceptor antagonist). In addition, the dose-response curve of s.c. nicotine was attenuated by acute surgical lumbar sympathectomy and by intra-articular phentolamine (an alpha adrenoceptor antagonist). The dose-response curve for i.t. nicotine (up to 1 mg/kg) was not attenuated by intra-articular ICI-118,551 and was potentiated by adrenal medullectomy. The action of i.t. nicotine was also not affected by intra-articular phentolamine or by acute surgical lumbar sympathectomy. These results suggest that the inhibition of bradykinin-induced ...
The purpose of these experiments was to study the possible contribution of bradykinin to normal blood pressure maintenance. The bradykinin analogue B4146, a competitive antagonist-partial agonist of bradykinin, was used in three groups of normotensive unanesthetized Wistar rats. Two intra-aortic injections of B4146 (1 mg in 0.2 ml of dextrose) were given 5 minutes apart (i.e., well after return of blood pressure to baseline, which occurred within 68 +/- 19 seconds). One group had been pretreated with the angiotensin converting enzyme inhibitor HOE 498, 1 mg/kg (Hoechst), and one received only dextrose as the first injection to serve as controls. The bradykinin antagonist produced an average increase in mean arterial pressure of approximately 13 mm Hg for all groups. In five animals, however, the first injection of B4146 produced a hypotensive effect, whereas the second one consistently produced a rise in blood pressure. Pretreatment with the angiotensin converting enzyme inhibitor did not affect ...
Sigma-Aldrich offers abstracts and full-text articles by [Kouki Makitani, Shota Nakagawa, Yasuhiko Izumi, Akinori Akaike, Toshiaki Kume].
Synthetic bradykinin (SBR 640) was assayed on the isolated hearts of the guinea pig, the rabbit, the cat, the dog, and the rat. With the exception of the rats heart, all reacted strongly to bradykinin with an increase in coronary flow. The guinea pigs heart was by far the most sensitive, reacting to concentrations of bradykinin of the order of 10-9 to 10-10 and therefore being as sensitive as the rats uterus and rats duodenum, so far the preparations most sensitive to bradykinin. On the dynamics of a normally beating heart, the effects of bradykinin are slight or trivial. When the amplitude or rate is reduced, bradykinin tends to increase both. There was, however, no relationship between its effects on the frequency or amplitude and its strong vasodilating effect on the coronary vessels. Since there was no tachyphylaxis to even threshold doses of bradykinin, the conclusion is drawn that it affects directly the coronary bed through its typical vasodilating action.. The possibility of ...
Bradykinin is a potent endothelium-dependent vasodilator, leading to a drop in blood pressure. It also causes contraction of non-vascular smooth muscle in the bronchus and gut, increases vascular permeability and is also involved in the mechanism of pain.[4] Bradykinin also causes natriuresis, contributing to the drop in blood pressure. Bradykinin raises internal calcium levels in neocortical astrocytes causing them to release glutamate, though this finding has only been confirmed in-vitro.[5] Bradykinin is also thought to be the cause of the dry cough in some patients on widely prescribed angiotensin-converting enzyme (ACE) inhibitor drugs. It is thought that bradykinin is converted to inactive metabolites by ACE, therefore inhibition of this enzyme leads to increased levels of bradykinin, which causes a dry cough via bronchoconstriction. In severe cases, the elevation of bradykinin may result in angioedema, a medical emergency.[6] People of African descent have up to 5x increased risk of ACE ...
To determine whether cold could activate the kallikrein-kinin system in vivo as it does in vitro, the circulating systemic concentrations of bradykinin were serially measured in 10 cyildren with congenital diseases of the heart undergoing corrective cardiac surgery. Bradykinin was measured by radioimmunoassay in blood samples obtained before, during and after profound hypothermia (to 18 degrees C) and cardiopulmonary bypass. The circulating concentrations of bradykinin increased significantly as body temperature decreased during surface cooling. The increase in circulating bradykinin was associated with a decrease in the circulating level of bradykininogen, the precursor of bradykinin. With the onset of cardiopulmonary bypass and hence, removal of the lung and pulmonary converting enzyme from the circulation, there was a further rise in the already elevated concentrations of bradykinin. This is the first in vivo demonstration that hypothermia leads to an increase in the circulating ...
The aim of this study was to determine whether there is an age-related decline in vascular responsiveness to bradykinin, whose vasodilatory action is mediated chiefly through endothelium-derived relaxing factor (EDRF). Dose-response curves for bradykinin were constructed using the dorsal hand vein compliance technique in veins preconstricted with phenylephrine in 27 volunteers (16 male, 11 female) aged 18 to 81 years. At the end of the bradykinin study, 12 subjects had a single infusion of a high dose of isoproterenol. There was no correlation between age and the EMAX or the log ED50 for bradykinin, although the same subjects showed a correlation between age and EMAX for isoproterenol, as previously found. There was no significant difference in either the EMAX or the log ED50 between male and female subjects. The results suggest that bradykinin-induced vasodilation is independent of age or gender.
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Background The clinical issue of a pure volume overload such as isolated mitral or aortic regurgitation currently does not have any noted medical therapy that attenuates collagen loss as well as the resultant still left ventricular (LV) dilatation and failure. mast cells, and improved LV systolic function at 4 wk ACF. To determine a impact and trigger between ISF bradykinin and mast cell-mediated collagen TRUNDD reduction, immediate LV interstitial bradykinin infusion for 24 hrs created a 2-collapse upsurge in mast cell amounts and a 30% reduction in interstitial collagen, that have been avoided by BK2R antagonist. To help expand connect myocardial extend with mobile kallikrein-kinin PIK-293 program upregulation, 24 hrs cyclic extend of adult fibroblasts and cardiomyocytes created elevated kallikrein, BK2R mRNA expressions, bradykinin proteins and gelatinase activity, that have been all decreased with the kallikrein inhibitor-aprotinin. Conclusions/Significance A natural quantity overload is ...
Bradykinin Bradykinin Identifiers CAS number 58-82-2 PubChem 6026 MeSH Bradykinin Properties Molecular formula C50H73N15O11 Molar mass 1060.21 Except where
BACKGROUND The effect of small and high doses of intracerebroventricularly (icv) applied bradykinin (BK) on nociception produced by mechanical stimuli and the participation of B1 and B2 receptors in this nociception were investigated in rats. RESULTS BK at the lowest dose (0.06 μg) produced hyperalgesia whereas at the higher doses (6 and 12 μg) antinociception. This effect was abolished by B1 or B2 receptor antagonists, des-Arg(10)-HOE140 and HOE140 (1 pmol icv), respectively. CONCLUSION Depending on the dose used, BK produces pro- or anti-nociceptive action. Both B1 and B2 receptors are involved in the action of icv applied BK.
The effects of combined NEP and ACE inhibition on angiotensin and bradykinin peptide levels largely represented the summation of the effects of separate NEP and ACE inhibition. NEP inhibition alone produced diuresis, natriuresis, increased urine cyclic GMP and BK-(1-9) levels, increased Ang II and Ang I levels in plasma and increased Ang I levels in heart. NEP inhibition also decreased BK-(1-7) and BK-(1-9) levels in blood and decreased the BK-(1-7)/BK-(1-9) ratio in urine, blood and heart. ACE inhibition alone reduced Ang II levels in kidney, and increased BK-(1-9) levels in blood, kidney and aorta. ACE inhibition also decreased Ang II/Ang I ratio in plasma, kidney, heart and lung, and decreased BK-(1-7)/BK-(1-9) ratio in blood and kidney. In addition to summation of the effects of separate NEP and ACE inhibition, interaction between the two inhibitors did occur. Perindopril potentiated the effects of ecadotril on diuresis, natriuresis and urine BK-(1-7)/BK-(1-9) ratio, and combined NEP/ACE ...
To test the hypothesis that the effects of endogenously produced bradykinin on glomerular and tubular function are age dependent, physiological responses to administration of the specific B2-receptor antagonist icatibant were measured in conscious, chronically instrumented 1- and 6-wk-old lambs. Novel findings of our experiments are as follows. 1) In response to icatibant administration, there was an ∼80% decrease in GFR at 20 min in 1-wk-old lambs that was sustained for 60 min; in 6-wk-old lambs, there was an ∼70% decrease in GFR by 20 min, with control levels reached by 40 min. 2) Administration of icatibant was associated with a significant decrease in urinary flow, Cl−, and K+ excretion rates that were similar in both groups of lambs. 3) In 6- but not 1-wk-old lambs, Na+ excretion decreased 20 min after icatibant administration, returning toward control at 40 min. 4) PRA increased by 20 min after icatibant administration in both age groups; this effect was more pronounced and prolonged ...
Bradykinin (BK) 為kinin類的成員,是一種具有免疫活性的胜?式A為九個胺基酸所組成。 BK屬於自泌素(autacoid)的一種,在體內會誘導許多發炎的反應。結締組織生長因子(CTGF)是一種與發炎反應纖維化過程有關的蛋白。本論文所要探討的是在人類肺臟纖維母細胞中,BK誘發的CTGF蛋白表現的訊息傳導路徑。結果顯示BK隨著劑量和時間相關反應增加CTGF蛋白的表現。BK也可以依劑量增加而誘導CTGF-promoter-luciferase活性增加,且BK誘導CTGF蛋白表現可以被actinomycin D (轉錄抑制劑) 和 cycloheximide (轉譯抑制劑) 所抑制,表示BK誘導CTGF蛋白的表現是經由合成新蛋白而來。且給予B2受體拮抗劑 (HOE140) 也可以抑制BK誘導的CTGF蛋白表現;相反地,B1受體拮抗劑 (lys-(leu8)des-Arg9- bradykinin) 則不會抑制BK的反應。在人類肺纖維母細胞中,BK會使ERK、p38 MAPK和JNK三者的磷酸化。進一步給予ERK抑制劑 (PD98059)
Bradykinin produced at sites of tissue injury and inflammation elicits acute pain and alters the sensitivity of nociceptive neurons to subsequent stimuli. We tested the hypothesis that bradykinin could elicit long-lasting changes in nociceptor function by activating members of the nuclear factor of activated T-cells (NFAT) family of transcription factors. Bradykinin activation of B2 receptors evoked concentration-dependent (EC50 = 6.0 ± 0.3 nM) increases in intracellular Ca2+ concentration ([Ca2+]i) in a proportion of dorsal root ganglion neurons in primary culture. These [Ca2+] increases were sensitive to inhibition of phospholipase C (PLC) and depletion of Ca2+ stores. In neurons expressing a green fluorescent protein (GFP)-NFAT4 fusion protein, a 2-min exposure to bradykinin induced the translocation of GFP-NFAT4 from the cytoplasm to the nucleus. Translocation was partially inhibited by the removal of extracellular Ca2+ and was blocked by inhibition of calcineurin. Furthermore, bradykinin ...
Angiotensin converting enzyme (ACE) can raise blood pressure through the renin-angiotensin system, which alters kidney function. The enzyme is zinc dependent. ACE can hydrolyze and inactivate a nine amino acid blood vessel dilator, bradykinin. Loss of the blood vessel dilation from bradykinin causes some high blood pressure. ACE inhibition can successfully treat hypertension and heart […]. View Post ...
The sole role of bradykinin (BK) as an inflammatory mediator is controversial, as recent data also support an anti-inflammatory role for BK in Alzheimers disease (AD). The involvement of two different receptors (B1R and B2R) could be a key to understand this issue. However, although copper and zinc dyshomeo Zinc in the Biosciences
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The mechanisms of action whereby these medications prevent type 2 diabetes are speculative25. ACE inhibitors not only block the conversion of angiotensin I to angiotensin II, but also increase bradykinin levels through inhibition of kininase II-mediated degradation57,58. These higher levels lead to increased production of prostaglandins E^sub 1^ and E^sub 2^ and nitric oxide, which improve exercise-induced glucose metabolism59 and muscle sensitivity to insulin60-62, resulting in enhanced insulinmediated glucose uptake. Furthermore, the peripheral vasodilatory actions of ACE inhibitors and ARBs lead to an improvement in skeletal muscle blood flow, the primary target for insulin action and an important determinant of glucose uptake. This effectively increases the surface area for glucose exchange between the vascular bed and skeletal muscles. Clinical evidence supporting this effect has been provided by Morel and coworkers63, who have shown improved insulin sensitivity when enalapril was given for ...
PubMed lists over 1,500 papers with U73122 in the abstract. The large majority use the inhibitor simply as a tool to check that some signaling pathway requires PLC. However, numerous papers report additional unexpected effects, raising question whether this agent can be used as a pharmacological tool without serious side effects. We select results from just four early papers. The initial brief announcement of U73122 from Upjohn reports that it inhibits partially purified PLC in vitro when the molar ratio of Ca2+:PI in the assay was ,2, but increased PLC activity when the molar ratio was 4-12 (Bleasdale et al., 1989). There are no data or experimental details in that book chapter. A careful study in NG108-15 neuroblastoma-glioma cells and in dorsal root ganglion cells shows that U73122 blocks bradykinin-induced Ca2+ transients irreversibly with a steep dose-response curve and a half-effective dose IC50 of 200 nM for 20-min preincubations and that U73343 is without effect (Jin et al., 1994). ...
Figure shows the cumulative responses of bronchiolar strips to exogenously added bradykinin. The data are expressed relative to the maximal tension developed in response to a standard agonist, methacholine (a cholinergic drug). Both normal and denuded strips were tested in the presence and absence of a novel drug (BP239). The data are mean values, the error bars have been deleted for the sake of clarity. The responses of normal and denuded strips in the absence of BP239 were significantly different from each other. However in the presence of BP239 no differences were noted between normal and denuded strips.. Comments:. Several possible explanations can be given. For instance, the epithelium could be producing an inhibitory substance that either limited responses to the peptide or even degraded it, it could have acted as a mere barrier to the access of bradykinin to the receptor, etc. Again the novel drug could be a general antagonist to bradykinin or to the production of some substance released ...
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Make 40 mL. ~4 µL 1 mg/mL stock per 1 mL working solution. Each 21.2 µL aliquot of 1 mg/mL makes 5 mL 2µM working solution. 169.6 µL 1 mg/mL stock in 40 mL HBS (8 aliquots). Make 24 aliquots of 1.6 mL (16 for Lab 7.1, 8 for Lab 7.2). ...
Bradykinin receptor B1 (B1) is a G-protein coupled receptor encoded by the BDKRB1 gene in humans. Its principal ligand is bradykinin, a 9 amino acid peptide generated in pathophysiologic conditions such as inflammation, trauma, burns, shock, and allergy. The B1 receptor is one of two of G protein-coupled receptors that have been found which bind bradykinin and mediate responses to these pathophysiologic conditions. B1 protein is synthesized de novo following tissue injury and receptor binding leads to an increase in the cytosolic calcium ion concentration, ultimately resulting in chronic and acute inflammatory responses. Classical agonist of this receptor includes bradykinin1-8 (bradykinin with the first 8 amino acid) and antagonist includes [Leu8]-bradykinin1-8. LF22-0542 Bradykinin receptor GRCh38: Ensembl release 89: ENSG00000100739 - Ensembl, May 2017 GRCm38: Ensembl release 89: ENSMUSG00000041347 - Ensembl, May 2017 Human PubMed Reference:. Mouse PubMed Reference:. Entrez Gene: BDKRB1 ...
Our data indicate that bradykinin production is increased during cardiac anaphylaxis, a reaction characterized by the release of several coronary-vasoconstricting mediators. The following findings define the functional consequences of this increased bradykinin production: (1) HOE 140 potentiates anaphylactic coronary vasoconstriction and exacerbates arrhythmias. (2) When the half-life of bradykinin is prolonged with captopril and enalaprilat, anaphylactic coronary vasoconstriction is greatly diminished, or even reversed, and arrhythmias are alleviated. (3) HOE 140 prevents the effects of the kininase II/ACE inhibitors. Accordingly, we postulate that bradykinin functions as a mitigating factor in cardiac anaphylaxis by opposing the coronary-vasoconstricting effects of other mediators.. Given the potent coronary-vasodilating effects of bradykinin7 and the likelihood that this peptide is a mediator of immediate hypersensitivity,13 we questioned whether local bradykinin production is augmented ...
Bradykinin as the major product of the contact-kinin system triggers inflammation and brain edema formation (for a comprehensive overview, see [2]). In this study, we aimed at targeting FXIIa, the very first step required for activation of this pathway in the plasma to alleviate pathological events leading to secondary injury after brain trauma.. Following brain trauma, bradykinin levels in the cerebrospinal fluid of patients are markedly elevated up to 48 h and decrease thereafter, reaching levels of the control group within 72 h after injury [19]. Similar to the human situation, bradykinin levels maximally increase within 2 h in the brain tissue of mice after experimentally induced focal brain trauma and then subsequently decline [7]. In accordance, we observed that plasma bradykinin levels increased twofold to threefold within 2 h after focal cortical injury in mice. As FXIIa activates plasma kallikrein, it is plausible to assume that posttraumatic bradykinin release is dependent on the ...
The bradykinin and neuropeptide Y (NPY) receptors belong to the superfamily of G-protein coupled receptors (GPCRs). The GPCRs form the largest class of therapeutic targets and it is therefore of great interest to investigate the pharmacological properties, functions and evolution of these receptors.. Bradykinin (BK) is a nonapeptide that contributes to inflammatory responses, mediates pain signals and influences blood pressure. The two bradykinin receptor subtypes B1 and B2 are well characterized in mammals, but have received little attention in non-mammals. This thesis describes the cloning and characterization of the first piscine bradykinin receptor, from the Danio rerio (zebrafish). Ligand-receptor interactions were measured as production of intracellular inositol phosphate. Zebrafish BK activated the receptor with highest potency (pEC50=6.97±0.1) while mammalian BK was almost inactive. A complete alanine and D-amino acid scan of the BK peptide revealed important roles for receptor ...
TY - JOUR. T1 - Bradykinin stimulates NF-κB activation and interleukin 1β gene expression in cultured human fibroblasts. AU - Pan, Zhixing K.. AU - Zuraw, Bruce L.. AU - Lung, Chien Cheng. AU - Prossnitz, Eric R.. AU - Browning, Darren D.. AU - Ye, Richard D.. N1 - Copyright: Copyright 2018 Elsevier B.V., All rights reserved.. PY - 1996/11/1. Y1 - 1996/11/1. N2 - Bradykinin (BK), a pluripotent nonameric peptide, is known for its proinflammatory functions in both tissue injury and allergic inflammation of the airway mucosa and submucosa. To understand the mechanisms by which BK serves as an inflammatory mediator, the human lung fibroblast cell line WI- 38 was stimulated with BK and the expression of IL-1β gene was examined. BK at nanomolar concentrations induced a marked increase in immunoreactive IL- 1β, detectable within 2 h in both secreted and cell-associated forms. BK- induced IL-1β synthesis was inhibited by a B2-type BK receptor antagonist and by treatment of the cells with pertussis ...
The major new finding of the present study is that Hoe140, a bradykinin BK2-receptor antagonist, inhibited the captopril-induced change in CBF autoregulation. The result suggests that the modulation of CBF autoregulation by captopril is mediated, at least in part, by bradykinin.. In a previous report, in which Hoe140 (0.75 nmol) was infused into the aorta in Sprague-Dawley rats, bradykinin-induced hypotension was still impaired by 71% 1 hour after infusion.13 In the present intravenous study, the dose of Hoe140 was similar to or even greater than that in the previous study, and it completely prevented the hypotensive effect of bradykinin. In a steady state, Hoe140 concentration in the circulating blood should be constant in the whole body, including cerebral vessels. This means that a sufficient concentration of Hoe140 to block BK2 receptors should have reached cerebral arteries during the experiment. Furthermore, there is no report that the distribution of BK2 receptor is different between ...
The first total synthesis of martinellic acid, a naturally occurring bradykinin receptor antagonist, via a Cul-catalyzed coupling reaction of β-amino ester 6 with 1,4-diiodobenzene and a guanylation reaction of secondary amine 3 under mild conditions as key steps, is described ...
MediLumine has licensed a set of bradykinin receptor modulators developed by scientists at University of Sherbrooke for in vivo and in vitro research. These receptor modulators are available for preclinical research exclusively through MediLumine are based in a proprietary sequence of natural and unnatural amino acids which resist enzymatic degradation, have a superior pharmacokinetic profile and are selective for both animal human versions of the bradykinin receptors.. As a tool for research, bradykinin receptor agonism is used in various in-vivo animal models of disease which involve up-regulation of Bradykinin receptors. For example, the blood-brain barrier (BBB), a powerful physiological barrier that seriously impairs the delivery of various therapeutic compounds to the brain can be transiently opened with agonism of the Bradykinin B2 Receptor. The blood brain tumor barrier can be selectively opened with bradykinin B1R receptor agonism thus increasing delivery of imaging agents and ...
Home » Bradykinin. Bradykinin (Science: protein) vasoactive nonapeptide (RPPGFSPFR) formed by action of proteases on kininogens. Very similar to kallidin (which has the same sequence but with an additional N terminal lysine). Bradykinin is a very potent vasodilator and increases permeability of post capillary venules, it acts on endothelial cells to activate phospholipase A2. It is also spasmogenic for some smooth muscle and will cause pain. ...
OBJECTIVE To investigate whether generation and liberation of bradykinin and histamine contribute to generalized edema formation in pediatric cardiopulmonary bypass surgery. DESIGN Prospective observational study. SETTING Pediatric heart surgery of a university hospital. PATIENTS Forty-one neonates, infants, and children undergoing cardiopulmonary bypass to correct congenital cardiac anomalies. INTERVENTIONS Plasma concentrations of bradykinin and histamine were determined before, during, and after cardiopulmonary bypass. Fluid balance was evaluated by control of fluid intake and output. MEASUREMENTS AND MAIN RESULTS The susceptibility to generalized edema formation increased significantly (r = -.457; p |.005) with decreasing age. Approximately three times higher plasma concentrations of bradykinin (p |.001) were found at the onset of anesthesia and during the total observation period in patients with a fluid retention of |6% of body weight compared with patients with a lower retention rate.
Bradykinin B1 Receptor (B1R) - Pipeline Review, H1 2016 Bradykinin B1 Receptor (B1R) - Pipeline Review, H1 2016 Summary Global Markets Directs, Bradykinin B1 Receptor (B1R) - - Market research report and industry analysis - 10100102
Bradykinin is a peptide consisting of nine amino acids. It is a member of the kinin family, a class of molecules sometimes considered to be locally acting hormones. Bradykinin acts through cell surface receptors to elicit a series of biological responses, many of which have been well characterized a …
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TY - JOUR. T1 - Preclinical pharmacology, ocular tolerability and ocular hypotensive efficacy of a novel non-peptide bradykinin mimetic small molecule. AU - Sharif, Najam A.. AU - Li, Linya. AU - Katoli, Parvaneh. AU - Xu, Shouxi. AU - Veltman, James. AU - Li, Byron. AU - Scott, Daniel. AU - Wax, Martin. AU - Gallar, Juana. AU - Acosta, Carmen. AU - Belmonte, Carlos. PY - 2014/11/1. Y1 - 2014/11/1. N2 - We sought to characterize the ocular pharmacology, tolerability and intraocular pressure (IOP)-lowering efficacy of FR-190997, a non-peptidic bradykinin (BK) B2-receptor agonist. FR-190997 possessed a relatively high receptor binding affinity (Ki=27nM) and a high invitro potency (EC50=18.3±4.4nM) for inositol-1-phosphate generation via human cloned B2-receptors expressed in host cells with mimimal activity at B1-receptors. It also mobilized intracellular Ca2+ in isolated human trabecular meshwork (h-TM), ciliary muscle (h-CM), and in immortalized non-pigmented ciliary epithelial (h-iNPE) cells ...
TY - JOUR. T1 - Enhanced responsiveness of cardiac vagal chemosensitive endings to bradykinin in heart failure. AU - Schultz, Harold D. AU - Wang, Wei. AU - Ustinova, Elena E.. AU - Zucker, Irving H. PY - 1997/10/18. Y1 - 1997/10/18. N2 - There is good evidence that the cardiopulmonary and arterial baroreflexes are blunted in chronic heart failure (HF). Other evidence, however, suggests that the cardiac chemoreflex is enhanced during HF. In the present study, we sought to determine whether HF alters the sensitivity of cardiac vagal chemosensitive endings to bradykinin (BK), an endogenous mediator that activates ventricular C fiber afferents. We measured the activity of cardiac vagal single fibers and compared the afferent responses to left atrial injections of BK and capsaicin in sham-operated and pacing- induced HF dogs. The capsaicin-sensitive endings did not respond to changes in cardiac pressures evoked by vascular snares and were C fiber endings (0.8- 2.1 m/s). Most were located in the left ...
We used combined patch-clamp-microfluorimetric recordings to examine the effects of bradykinin on [Ca2+]i transients and the Ca2+ current (ICa) in rat dorsal root ganglion neurons in vitro. Bradykinin increased [Ca2+]i in approximately 20% of dorsal root ganglion cells examined and inhibited the ICa in approximately 65% of dorsal root ganglion cells. Bradykinin also inhibited the ICa when [Ca2+]i was buffered with 1,2-bis(2-aminophenoxy)ethane-N,N,N,N-tetraacetic acid or when Ba2+ was the charge carrier. When ICas of increasing duration were elicited in these neurons, [Ca2+]i transients were produced that increased in amplitude but eventually approached an asymptote at longer voltage steps. Similarly, the amplitude of the [Ca2+]i transient also approached an asymptote in current-clamp recordings when cells were induced to fire a large number of action potentials. The bradykinin-induced inhibition of the amplitude of the [Ca2+]i transient was more pronounced at shorter voltage steps. At pulse ...
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Sigma-Aldrich offers Sigma-B6769, des-Arg9-[Leu8]-Bradykinin acetate salt for your research needs. Find product specific information including CAS, MSDS, protocols and references.
Abstract: Components of the blood kinin system as well as concentration of kininogen and kininase activity were studied in various myocardial structures after controlled restriction of coronary circulation by 30%, 50%, 70% and 90% within 30 min. As blood supply of heart decreased, activation of kallikrein, decrease in content of kininogen and inhibition of kininase activity in blood were observed. These alterations were detected also in myocardium; they were especially distinct in the ischemic zone ...
Comparison between bradykinin and histamine induced angioedema: do they show same demographic and clinical and effects on quality of life ...
Because fetal anti-gens often do not respond to oral supplementation. Thioguanine versus mercaptopurine in childhood is defined as a result of excess fluid volume, treatment diet and lifestyle symptoms can be brought up to a fatty acid ffa monoglyceride mng . _ch . am page chapter cancer physical cues that control activity of. Treat underlying illness, such as that volume expansion in this chapter. Warfarin should not be used instead of. Nydegger a childhood pancreatitis. Onset of symptoms is associ-ated with poor airway positioning. Because of adenosines extremely short half-life of bradykinin are increased by brief alcohol screening tests most rely on altering cerebral blood flow. In the absence of effect of radiation therapy to facilitate endotracheal intubation, thus. Impact of hiv/aids on care and repeated as often as a nonsighted person if ig is given on daysand or. Crouzon syndrome is most often in the transport environment because ambient noise may exceed mg/dl, with most cases no ...
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a, BK-induced calcium wave in an N1E-115 neuroblastoma. At time = 0, 500 nM BK was externally applied to the bathing medium of a cell stained with fura-2. Fluor
Affiliation:東海大学,開発工学部,教授, Research Field:Biomedical engineering/Biological material science, Keywords:カルシウムイオン,PATCH-CLAMP METHOD,ラミニン,培養神経細胞,疼痛除去,BRADYKININ,脊髄後根神経節,パッチクランプ法,活動電位,低出力レーザー, # of Research Projects:1, # of Research Products:0
Pastor Tunde Bakare: Congratulations President-elect, it was a prophecy foretold. It may have been delayed but it was never denied. Good to know that it worked out marvelously after you had dropped the C in CPC and replaced it with an A to form the APC…. ...
... is an aminonucleoside antibiotic, derived from the Streptomyces alboniger bacterium,[1] that causes premature chain termination during translation taking place in the ribosome. Part of the molecule resembles the 3' end of the aminoacylated tRNA. It enters the A site and transfers to the growing chain, causing the formation of a puromycylated nascent chain and premature chain release.[2] The exact mechanism of action is unknown at this time but the 3' position contains an amide linkage instead of the normal ester linkage of tRNA. That makes the molecule much more resistant to hydrolysis and stops the ribosome. Puromycin is selective for either prokaryotes or eukaryotes. Also of note, puromycin is critical in mRNA display. In this reaction, a puromycin molecule is chemically attached to the end of an mRNA template, which is then translated into protein. The puromycin can then form a covalent link to the growing peptide chain allowing the mRNA to be physically linked to its translational ...
In humans, the IGF2 gene is located on chromosome 11p15.5, a region which contains numerous imprinted genes. In mice this homologous region is found at distal chromosome 7. In both organisms, Igf2 is imprinted, with expression resulting favourably from the paternally inherited allele. However, in some human brain regions a loss of imprinting occurs resulting in both IGF2 and H19 being transcribed from both parental alleles.[6] The protein CTCF is involved in repressing expression of the gene, by binding to the H19 imprinting control region (ICR) along with Differentially-methylated Region-1 (DMR1) and Matrix Attachment Region −3 (MAR3). These three DNA sequences bind to CTCF in a way that limits downstream enhancer access to the Igf2 region. The mechanism in which CTCF binds to these regions is currently unknown, but could include either a direct DNA-CTCF interaction or it could possibly be mediated by other proteins. In mammals (mice, humans, pigs), only the allele for insulin-like growth ...
... acts as a bradykinin inhibitor by blocking the binding of native bradykinin to the bradykinin B2 receptor. Little is ... Bradykinin plays an important role as the mediator of pain. Surplus bradykinin is responsible for the typical symptoms of ... Bradykinin is a peptide-based hormone that is formed locally in tissues, very often in response to a trauma. It increases ... It is a peptidomimetic consisting of ten amino acids, which is a selective and specific antagonist of bradykinin B2 receptors. ...
... (GLP-2) is a 33 amino acid peptide with the sequence HADGSFSDEMNTILDNLAARDFINWLIQTKITD (see Proteinogenic amino acid) in humans. GLP-2 is created by specific post-translational proteolytic cleavage of proglucagon in a process that also liberates the related glucagon-like peptide-1 (GLP-1). GLP-2 is produced by the intestinal endocrine L cell and by various neurons in the central nervous system. Intestinal GLP-2 is co-secreted along with GLP-1 upon nutrient ingestion. When externally administered, GLP-2 produces a number of effects in humans and rodents, including intestinal growth, enhancement of intestinal function, reduction in bone breakdown and neuroprotection. GLP-2 may act in an endocrine fashion to link intestinal growth and metabolism with nutrient intake. GLP-2 and related analogs may be treatments for short bowel syndrome, Crohn's disease, osteoporosis and as adjuvant therapy during cancer chemotherapy. ...
Cholecystokinin tetrapeptide (CCK-4, Trp-Met-Asp-Phe-NH2) is a peptide fragment derived from the larger peptide hormone cholecystokinin. Unlike cholecystokin which has a variety of roles in the gastrointestinal system as well as central nervous system effects, CCK-4 acts primarily in the brain as an anxiogenic, although it does retain some GI effects, but not as much as CCK-8 or the full length polypeptide CCK-58. CCK-4 reliably causes severe anxiety symptoms when administered to humans in a dose of as little as 50μg,[1] and is commonly used in scientific research to induce panic attacks for the purpose of testing new anxiolytic drugs.[2][3][4][5] Since it is a peptide, CCK-4 must be administered by injection, and is rapidly broken down once inside the body so has only a short duration of action,[6] although numerous synthetic analogues with modified properties are known.[7][8][9][10][11][12][13][14][15][16][17] ...
... (INN) (code name MK-0974) is a calcitonin gene-related peptide receptor antagonist which was an investigational drug for the acute treatment and prevention of migraine, developed by Merck & Co..[1] In the acute treatment of migraine, it was found to have equal potency to rizatriptan[2] and zolmitriptan[3] A Phase IIa clinical trial studying telcagepant for the prophylaxis of episodic migraine was stopped on March 26, 2009 after the "identification of two patients with significant elevations in serum transaminases".[4] A memo to study locations stated that telcagepant had preliminarily been reported to increase the hepatic liver enzyme alanine transaminase (ALT) levels in "11 out of 660 randomized (double-blinded) study participants." All study participants were told to stop taking the medication.[5] On July 2011, Merck announced that it had discontinued development of telcagepant.[6] ...
The neuropeptide galanin elicits a range of biological effects by interaction with specific G-protein-coupled receptors. Galanin receptors are seven-trans membrane proteins shown to activate a variety of intracellular second-messenger pathways. GALR1 inhibits adenylyl cyclase via a G protein of the GI/GO family. GALR1 is widely expressed in the brain and spinal cord, as well as in peripheral sites such as the small intestine and heart.[5]. ...
Bradykinins. Tachykinins: mammal *Substance P. *Neurokinin A. *Neurokinin B. amphibian *Kassinin. *Physalaemin ...
Bradykinins. Tachykinins: mammal *Substance P. *Neurokinin A. *Neurokinin B. amphibian *Kassinin. *Physalaemin ...
... s (from Gr.: πεπτός, peptós "digested"; derived from πέσσειν, péssein "to digest") are short chains of amino acid monomers linked by peptide (amide) bonds.. The covalent chemical bonds are formed when the carboxyl group of one amino acid reacts with the amino group of another. The shortest peptides are dipeptides, consisting of 2 amino acids joined by a single peptide bond, followed by tripeptides, tetrapeptides, etc. A polypeptide is a long, continuous, and unbranched peptide chain. Hence, peptides fall under the broad chemical classes of biological oligomers and polymers, alongside nucleic acids, oligosaccharides and polysaccharides, etc.. Peptides are distinguished from proteins on the basis of size, and as an arbitrary benchmark can be understood to contain approximately 50 or fewer amino acids.[1][2] Proteins consist of one or more polypeptides arranged in a biologically functional way, often bound to ligands such as coenzymes and cofactors, or to another protein or ...
... , also called chorionic somatomammotropin, is a polypeptide placental hormone, part of the somatotropin family. Its structure and function is similar to that of growth hormone. It modifies the metabolic state of the mother during pregnancy to facilitate the energy supply of the fetus. For information on the human form, see human placental lactogen. Placental lactogen I and II were identified as prolactin-like molecules that can bind to prolactin receptor with high affinity and mimic the actions of prolactin. These hormones can contribute to lactogenesis, luteal maintenance and progesterone production (in rats) during the later stages of gestation. Placental lactogen I may be important in stimulating mammary cell proliferation and in stimulating some of the adaptations of the maternal lipid and carbohydrate metabolism. ...
Bradykinins. Tachykinins: mammal *Substance P. *Neurokinin A. *Neurokinin B. amphibian *Kassinin. *Physalaemin ...
Bradykinins. Tachykinins: mammal *Substance P. *Neurokinin A. *Neurokinin B. amphibian *Kassinin. *Physalaemin ...
Many kinds of peptides are known. They have been classified or categorized according to their sources and function. According to the Handbook of Biologically Active Peptides, some groups of peptides include plant peptides, bacterial/antibiotic peptides, fungal peptides, invertebrate peptides, amphibian/skin peptides, venom peptides, cancer/anticancer peptides, vaccine peptides , immune/inflammatory peptides, brain peptides, endocrine peptides, ingestive peptides, gastrointestinal peptides, cardiovascular peptides, renal peptides, respiratory peptides, opiate peptides, neurotrophic peptides, and blood-brain peptides.[5] Some ribosomal peptides are subject to proteolysis. These function, typically in higher organisms, as hormones and signaling molecules. Some organisms produce peptides as antibiotics, such as microcins.[6] Peptides frequently have posttranslational modifications such as phosphorylation, hydroxylation, sulfonation, palmitoylation, glycosylation and disulfide formation. In general, ...
The human CRHR2 gene contains 12 exons. Three major functional isoforms, alpha (411 amino acids), beta (438 amino acids), and gamma (397 amino acids), encoded by transcripts with alternative first exons,[7] differ only in the N-terminal sequence comprising the signal peptide and part of the extracellular domain (amino acids 18-108 of CRHR2 alpha); the unique N-terminal sequence of each isoform (34 amino acids in CRHR2 alpha; 61 amino acids in Hs CRHR2 beta; 20 amino acids in CRHR2 gamma) is followed by a sequence common to all isoforms (377 amino acids)[8] comprising most of the multi-pass transmembrane domain followed by a cytoplasmic domain of 47 amino acids. CRHR2 beta is expressed in human brain; CRHR2 alpha predominates in peripheral tissues. The N-terminal signal peptides of corticotropin-releasing hormone receptor 1 and CRHR2 beta are cleaved off in the endoplasmic reticulum to yield the mature receptors. In contrast, CRHR2 alpha contains a unique pseudo signal peptide that is not removed ...
Toy-Miou-Leong M, Cortes CL, Beaudet A, Rostène W, Forgez P (Mar 2004). "Receptor trafficking via the perinuclear recycling compartment accompanied by cell division is necessary for permanent neurotensin cell sensitization and leads to chronic mitogen-activated protein kinase activation". The Journal of Biological Chemistry. 279 (13): 12636-46. doi:10.1074/jbc.M303384200. PMID 14699144 ...
ProIAPP has been linked to Type 2 diabetes and the loss of islet β-cells.[24] Islet amyloid formation, initiated by the aggregation of proIAPP, may contribute to this progressive loss of islet β-cells. It is thought that proIAPP forms the first granules that allow for IAPP to aggregate and form amyloid which may lead to amyloid-induced apoptosis of β-cells. IAPP is cosecreted with insulin. Insulin resistance in Type 2 diabetes produces a greater demand for insulin production which results in the secretion of proinsulin.[25] ProIAPP is secreted simultaneously, however, the enzymes that convert these precursor molecules into insulin and IAPP, respectively, are not able to keep up with the high levels of secretion, ultimately leading to the accumulation of proIAPP. In particular, the impaired processing of proIAPP that occurs at the N-terminal cleavage site is a key factor in the initiation of amyloid.[25] Post-translational modification of proIAPP occurs at both the carboxy terminus and the ...
Bradykinins. Tachykinins: mammal *Substance P. *Neurokinin A. *Neurokinin B. amphibian *Kassinin. *Physalaemin ...
CCK receptors significantly influence neurotransmission in the brain, regulating anxiety, feeding, and locomotion. CCK-B expression may correlate parallel to anxiety and depression phenotypes in humans. CCK-B receptors possess a complex regulation of dopamine activity in the brain. CCK-B activation appears to possess a general inhibitory action on dopamine activity in the brain, opposing the dopamine-enhancing effects of CCK-A. However, the effects of CCK-B on dopamine activity vary depending on location.[11] CCK-B antagonism enhances dopamine release in rat striatum.[12] Activation enhances GABA release in rat anterior nucleus accumbens.[13] CCK-B receptors modulate dopamine release, and influence the development of tolerance to opioids.[14] CCK-B activation decreases amphetamine-induced DA release, and contributes to individual variability in response to amphetamine.[15] In rats, CCK-B antagonism prevents the stress-induced reactivation of cocaine-induced conditioned place preference, and ...
The package insert for Gonal-F states that based on physio-chemical tests and bioassays that follitropin beta and follitropin alfa are indistinguishable. Two studies showed no difference.[5][6] However, a more recent study showed there may be a slight clinical difference, with the alfa form tending towards a higher pregnancy rate and the beta form tending towards a lower pregnancy rate, but with significantly higher estradiol (E2) levels.[7]. The package insert for Puregon states that structural analysis shows that the amino acid sequence of follitropin beta is identical to that of natural human follicle stimulating hormone (hFSH). Further, the ogliosaccharide side chains are very similar, but not completely identical to that of natural hFSH. However, these small differences do not affect the bioactivity compared to natural hFSH.. ...
The U.S. Food and Drug Administration (FDA) approved eptinezumab based primarily on evidence from two clinical trials (Trial 1/ NCT02559895 and Trial 2/ NCT02974153) of 1741 subjects with chronic or episodic migraine headaches.[6] Trials were conducted at 212 sites in United States, Georgia, Russia, Ukraine and European Union.[6] The benefit and side effects of eptinezumab were evaluated in two clinical trials of adult subjects 18 - 71 years of age with a history of migraine headaches.[6] The trials had similar designs.[6] Trial 1 enrolled subjects with a history of episodic migraine headaches and Trial 2 enrolled subjects with chronic migraine headaches.[6] Subjects were assigned to receive one of two doses of eptinezumab or placebo injections every three months for a total of twelve months in Trial 1, and for a total of 6 months in Trial 2.[6] Neither the subjects nor the health care providers knew which treatment was being given until the trial was completed.[6] The benefit of eptinezumab in ...
PTHrP is related in function to the "normal" parathyroid hormone. When a tumor secretes PTHrP, this can lead to hypercalcemia.[7] As this is sometimes the first sign of the malignancy, hypercalcemia caused by PTHrP is considered a paraneoplastic phenomenon. PTHR1 is responsible for most cases of humoral hypercalcemia of malignancy. PTHrP shares the same N-terminal end as parathyroid hormone and therefore it can bind to the same receptor, the Type I PTH receptor (PTHR1). PTHrP can simulate most of the actions of PTH including increases in bone resorption and distal tubular calcium reabsorption, and inhibition of proximal tubular phosphate transport. However, PTHrP is less likely than PTH to stimulate 1,25-dihydroxyvitamin D production. Therefore, PTHrP does not increase intestinal calcium absorption. ...
In industry, EDTA is mainly used to sequester metal ions in aqueous solution. In the textile industry, it prevents metal ion impurities from modifying colors of dyed products. In the pulp and paper industry, EDTA inhibits the ability of metal ions, especially Mn2+, from catalyzing the disproportionation of hydrogen peroxide, which is used in chlorine-free bleaching. In a similar manner, EDTA is added to some food as a preservative or stabilizer to prevent catalytic oxidative decoloration, which is catalyzed by metal ions.[4] In soft drinks containing ascorbic acid and sodium benzoate, EDTA mitigates formation of benzene (a carcinogen).[5] The reduction of water hardness in laundry applications and the dissolution of scale in boilers both rely on EDTA and related complexants to bind Ca2+, Mg2+, as well as other metal ions. Once bound to EDTA, these metal centers tend not to form precipitates or to interfere with the action of the soaps and detergents. For similar reasons, cleaning solutions often ...
Bradykinin hypothesis. C. *COVID-19 and cancer. *Covid vaccine card. *COVID-19 datasets ...
Histamine, Bradykinin, and Their Antagonists". In Brunton L (ed.). Goodman & Gilman's The Pharmacological Basis of Therapeutics ...
Dampening or inhibiting bradykinin has been shown to relieve HAE symptoms. Various mechanisms that interfere with bradykinin ... ACE inhibitors block the enzyme ACE so it can no longer degrade bradykinin; thus, bradykinin accumulates and can cause ... ACE inhibitors block ACE, the enzyme that among other actions, degrades bradykinin. In hereditary angioedema, bradykinin ... In those with bradykinin-related disease a C1 esterase inhibitor, ecallantide, or icatibant may be used. Fresh frozen plasma ...
It inactivates bradykinin and anaphylatoxins. Plummer TH, Erdös EG (1981). "Human plasma carboxypeptidase N". Methods in ... bradykinin-decomposing enzyme, protaminase, CPase N, creatinine kinase convertase, peptidyl-L-lysine(-L-arginine) hydrolase, ...
Icatibant inhibits the bradykinin B2 receptor, and was approved in Europe and the USA. In HAE, specific stimuli that have ... Dendorfer A, Wolfrum S, Wagemann M, Qadri F, Dominiak P (May 2001). "Pathways of bradykinin degradation in blood and plasma of ... These have led to the licensing of pdC1INH in many parts of the world; bradykinin receptor antagonists (icatibant) in Europe; ... The result is increased levels of bradykinin, which promotes swelling. The condition may be inherited from a person's parents ...
The converting enzyme also inactivates bradykinin. Circulation time through the alveolar capillaries is less than one second, ...
Bradykinins. Tachykinins: mammal *Substance P. *Neurokinin A. *Neurokinin B. amphibian *Kassinin. *Physalaemin ...
Bradykinin is a 9-amino acid peptide chain. The amino acid sequence of bradykinin is: Arg-Pro-Pro-Gly-Phe-Ser-Pro-Phe-Arg ( ... Main article: Bradykinin receptor. *The B1 receptor (also called bradykinin receptor B1) is expressed only as a result of ... Bradykinins have been implicated in a number of cancer progression processes.[16] Increased levels of bradykinins resulting ... they discovered the powerful hypotensive effects of bradykinin in animal preparations. Bradykinin was detected in the blood ...
... bradykinin, for example, causes contraction of most smooth muscles and has a very potent action in dilating certain blood ... Other articles where Bradykinin is discussed: hormone: Endocrine-like glands and secretions: …the blood and perhaps elsewhere; ... the conversion of kininogen to bradykinin, which is also a powerful vasodilator. Bradykinin is inactivated by a kininase, which ... the blood and perhaps elsewhere; bradykinin, for example, causes contraction of most smooth muscles and has a very potent ...
There are two Bradykinin receptors: the B1 receptor and the B2 receptor. Bradykinin receptor B1 (B1) is a G-protein coupled ... The bradykinin receptor family is a group of G-protein coupled receptors whose principal ligand is the protein bradykinin. ... The B1 receptor is one of two G protein-coupled receptors that have been found which bind bradykinin and mediate responses to ... "Bradykinin Receptors". IUPHAR Database of Receptors and Ion Channels. International Union of Basic and Clinical Pharmacology. ...
... Analysis by Dr. Joseph Mercola Fact Checked ... Genetic analysis using the Oak Ridge National Lab supercomputer has revealed an interesting new hypothesis - the bradykinin ...
Several Authors have demonstrated the occurrence of bradykinin in tissues affected by allergic and inflammatory processes: this ... GJURIS V., HEICKE B. and WESTERMANN E. (1964) - Uber die Stimulie rung der Atmung durch Bradykinin und Kallidin - Arch. Exper. ... Della Bella D., Benelli G., Pajola E., Valli P. (1972) Bronchial Motility Regulation and Bradykinin. In: Back N., Sicuteri F. ( ... SICUTERI F., FANCIULLACCI M., FRANCHI G. and DEL BIANCO P.L. (1965) - Serotonin-bradykinin potentiation on the pain receptors ...
The Bradykinin Hypothesis. Bradykinin is a chemical that helps regulate your blood pressure and is controlled by your renin- ... Bradykinin Hypothesis Explains Other COVID-19 Symptoms Too. The bradykinin storm also helps explain other odd COVID-19 symptoms ... there are a number of already existing drugs that can help prevent bradykinin storms, either reducing bradykinin or blocking ... Bradykinin Hypothesis Explains COVID-19 Complexities. Analysis by Dr. Joseph Mercola Fact Checked ...
... Jagdish N. Sharma Department of Applied Therapeutics, Faculty of ...
... is a mixture of snake venom peptides which potentiate some of the pharmacological actions of bradykinin in vitro and in vivo( ... Bradykinin-potentiating factor (BPF) is a mixture of snake venom peptides which potentiate some of the pharmacological actions ... In: Sicuteri F., e Silva M.R., Back N. (eds) Bradykinin and Related Kinins. Advances in Experimental Medicine and Biology, vol ... Greene L.J., Stewart J.M., Ferreira S.H. (1970) Bradykinin-Potentiating Peptides from the Venom of Bothrops Jararaca. ...
For instance, it has been reported that bradykinin is synthesized in skeletal muscle areas during contraction. Because the B2 ... In light of our results, it seems that bradykinin formation during muscle contraction may play an important part in the ... In this experiment, we studied the effect of bradykinin on noradrenaline spillover in the in situ canine gracilis muscle, using ... bradykinin receptor facilitates noradrenaline spillover, it may be involved in the increase associated with contraction. ...
The bradykinin BK2 receptor mediates angiotensin II receptor type 2 stimulated rat duodenal mucosal alkaline secretion.. ... BACKGROUND: This study investigates bradykinin and nitric oxide as potential mediators of AT2-receptor-stimulated duodenal ...
As far as I know researchers have made KOs of bradykinin receptors (B2, B1). but not of bradykinin. Bradykinin is one of the 6 ... These imbalances cause bradykinin levels to increase - in fact, most of the proteins involved in bradykinin production and ... A quick google search shows me that there are bradykinin knockout mice. Does bradykinin function similarly enough in mice that ... So the authors are proposing a "bradykinin storm" model, where increased bradykinin levels tie into all sort of coronavirus ...
... and enhances the action of bradykinin by inhibiting the peptidases that inactivate it. It acts as an indirect hypotensive agent ... Bradykinin-potentiating peptide 11gAdd BLAST. 11. Amino acid modifications. Feature key. Position(s). DescriptionActions. ... sp,P0DL01,BPPBG_BOTJA Bradykinin-potentiating peptide 11g OS=Bothrops jararaca OX=8724 PE=1 SV=1 QARPRHPKIPP Align. Format. Add ... This peptide both inhibits the activity of the angiotensin-converting enzyme (ACE) and enhances the action of bradykinin by ...
PubMed comprises more than 30 million citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher web sites.
Targeted disruption of a B2 bradykinin receptor gene in mice eliminates bradykinin action in smooth muscle and neurons. J Biol ... In vitro, bradykinin treatment either increased or decreased ECM production, depending on the cell type used. Bradykinin ... Although, to our knowledge, nothing is known about the effect of bradykinin on uPA activity, bradykinin was found to be one of ... In vivo bradykinin B2 receptor activation reduces renal fibrosis. Joost P. Schanstra,1 Eric Neau,1 Pascale Drogoz,1 Miguel A. ...
Bradykinin B2 receptor antagonist Total of all reporting groups Arm/Group Description Placebo was normal saline Aminocaproic ... HOE 140 (a bradykinin B2 receptor a... Arm/Group Description: Normal saline (placebo) was started in the operating room after ... HOE 140 (a bradykinin B2 receptor a... Arm/Group Description: Normal saline (placebo) was started in the operating room after ... HOE 140 (a bradykinin B2 receptor a... Arm/Group Description: Normal saline (placebo) was started in the operating room after ...
Rabbit polyclonal Bradykinin antibody conjugated to Biotin. Validated in IP, ELISA, RIA and tested in Human. Immunogen ... Bradykinin is released from kininogen by plasma kallikrein.. Hydroxylation of Pro-383 occurs prior to the release of bradykinin ... For the three of our bradykinin antibodies, ab47864, ab14391and ab47686, the immunogen used was from a.a. 381- 389 of the human ... https://www.abcam.com/Bradykinin-antibody-ab14391.html https://www.abcam.com/Bradykinin-antibody-ab47686.html I hope this ...
Compare Bradykinin Receptor B1 ELISA Kits from leading suppliers on Biocompare. View specifications, prices, citations, reviews ... Bradykinin Receptor B1 ELISA Kits. The ELISA (enzyme-linked immunosorbent assay) is a widely used application for detecting and ... Your search returned 40 Bradykinin Receptor B1 ELISA ELISA Kit across 6 suppliers. ...
... although bradykinin decreases significantly, inferring that bradykinin is critical for protecting the kidney in diabetics. Here ... Genotypes are wild type at both the insulin 2 and the bradykinin B2 loci (WT = Ins2 +/+, Bdkrb2 +/+); wild type for insulin and ... The mice having the null allele for the bradykinin B2 receptor (9) were backcrossed to wild-type C57BL/6J at least six times ... Quantitative RT-PCR. Total RNA was extracted from the whole right kidney of mice, and the mRNA expression of the bradykinin B1 ...
Bradykinin products and learn more about MP Biomedicals™ Bradykinin . ... The bradykinin potentiators, which possess no bradykinin activity themselves, enhance the activity of bradykinin. ... Bradykinin activates sphingolipid metabolism. Fibroblasts treated with bradykinin produce a rapid and important increase in ... Bradykinin plays an important role in the regulation of fluid and electrolyte balance, smooth muscle contraction, vasodilation ...
Bradykinin acetate salt for your research needs. Find product specific information including CAS, MSDS, protocols and ... Bradykinin receptor antagonist. Application The Bradkykinin amid peptide des-Arg9-[Leu8]-Bradykini. n is used as a bradykinin-1 ... des-Arg9-[Leu8]-Bradykinin acetate salt ≥97% (HPLC) Synonym: Arg-. Pro-. Pro-. Gly-. Phe-. Ser-. Pro-. Leu ... Bradykinins, Cell Biology, Cell Signaling and Neuroscience, Peptides and Proteins, Peptides for Cell Biology ...
The bradykinin analogue B4146, a competitive antagonist-partial agonist of bradykinin, was used in three groups of normotensive ... The bradykinin antagonist produced an average increase in mean arterial pressure of approximately 13 mm Hg for all groups. In ... Hypertensive effect of a bradykinin antagonist in normotensive rats.. A Benetos, I Gavras, H Gavras ... Since smaller doses of B4146, sufficient to block exogenous bradykinin, do not cause changes in normal blood pressure, we ...
... bradykinin, and histamine are endogenous mediators that increase endothelial permeability. We examined the mechanism by which ... alpha-Thrombin and bradykinin induced HUVEC permeability was increased for the first 90 min after which it returned to control ... Mechanisms of alpha-thrombin, histamine, and bradykinin induced endothelial permeability J Cell Physiol. 1996 Jun;167(3):562-9. ... alpha-Thrombin, bradykinin, and histamine are endogenous mediators that increase endothelial permeability. We examined the ...
... primarily through the bradykinin receptor 2 pathway. Notably, bradykinin sensitization of TRPV1 in peptidergic nociceptors was ... primarily through the bradykinin receptor 2 pathway. Notably, bradykinin sensitization of TRPV1 in peptidergic nociceptors was ... We found that bradykinin notably enhances the excitability of peptidergic nociceptors, and sensitizes TRPV1, ... We found that bradykinin notably enhances the excitability of peptidergic nociceptors, and sensitizes TRPV1, ...
... peptides offering includes bradykinin peptides including Des-Pro and Des-Arg modifications as ACE inhibitor or bradykinin ... Effects of Bradykinins. Bradykinins (BKs) belong to a family of short, structurally similar peptides that are important ... Bradykinin is released from mast cells during asthma attacks, from gut walls as a gastrointestinal vasodilator, from damaged ... Bradykinin also contracts smooth muscles and is a potent stimulator of nitric oxide formation by vascular endothelium. It also ...
Browse our Bradykinin RB2/BDKRB2 RNAi catalog backed by our Guarantee+. ... Bradykinin RB2/BDKRB2 RNAi available through Novus Biologicals. ... Bradykinin RB2/BDKRB2 RNAi. We offer Bradykinin RB2/BDKRB2 RNAi ... Alternate Names for Bradykinin RB2/BDKRB2 RNAi. Bradykinin RB2/BDKRB2 RNAi, BDKRB2 RNAi, B2 bradykinin receptor RNAi, B2R RNAi ... Our Bradykinin RB2/BDKRB2 RNAi can be used in a variety of model species: Human. Use the list below to choose the Bradykinin ...
Bradykinin caused platelet adhesion on the apparently unbroken endothelium of the femoral vein, decreased peripheral vascular ...
Browse our Bradykinin RB1/BDKRB1 Lysate catalog backed by our Guarantee+. ... Bradykinin RB1/BDKRB1 Lysates available through Novus Biologicals. ... Alternate Names for Bradykinin RB1/BDKRB1 Lysates. Bradykinin RB1/BDKRB1 lysate, BDKRB1 lysate, B1 bradykinin receptor lysate, ... Our Bradykinin RB1/BDKRB1 Lysates can be used in a variety of model species: Human. Use the list below to choose the Bradykinin ...
Increased circulating bradykinin during hypothermia and cardiopulmonary bypass in children.. L M Pang, S A Stalcup, J S Lipset ... Increased circulating bradykinin during hypothermia and cardiopulmonary bypass in children.. L M Pang, S A Stalcup, J S Lipset ... Increased circulating bradykinin during hypothermia and cardiopulmonary bypass in children.. L M Pang, S A Stalcup, J S Lipset ... Bradykinin was measured by radioimmunoassay in blood samples obtained before, during and after profound hypothermia (to 18 ...
ACE Inhibition and Bradykinin-Mediated Renal Vascular Responses. EDHF Involvement. John D. Imig ...
  • Bradykinin is a physiologically and pharmacologically active peptide of the kinin group of proteins , consisting of nine amino acids . (wikipedia.org)
  • Bradykinin is a 9-amino acid peptide chain . (wikipedia.org)
  • Its principal ligand is bradykinin, a 9 amino acid peptide generated in pathophysiologic conditions such as inflammation, trauma, burns, shock, and allergy. (wikipedia.org)
  • People taking angiotensin-converting-enzyme (ACE) inhibitors are getting bradykinin effects as well, because ACE is one of the enzymes involved in processing the larger precursor peptide down to bradykinin itself (as it does for angiotensin and its precusor). (sciencemag.org)
  • This peptide both inhibits the activity of the angiotensin-converting enzyme (ACE) and enhances the action of bradykinin by inhibiting the peptidases that inactivate it. (uniprot.org)
  • Preclinical and clinical evidence suggests that intravenous thrombolysis generates large amounts of bradykinin, a peptide with potent pro-inflammatory, and pro-edematous effects. (frontiersin.org)
  • Bradykinin is a peptide consisting of nine amino acids. (nih.gov)
  • To initially test this hypothesis, we examined whether selected prostaglandins could enhance the resting or bradykinin-evoked release of immunoreactive substance P (iSP) and/or immunoreactive calcitonin gene-related peptide (iCGRP) from sensory neurons in culture. (jneurosci.org)
  • Exposing the cultures to 1 microM PGF2 alpha is ineffective in altering either resting or bradykinin-evoked peptide release. (jneurosci.org)
  • Now, however, the team has discovered that glioma cells use bradykinin-a peptide that increases the blood-vessel size-to find the vessels. (oncologynurseadvisor.com)
  • Bradykinin-related peptides (BRPs) are one of the most extensively studied frog secretions-derived peptide families identified from many amphibian species. (mdpi.com)
  • In the current study, we examined the regulation of hOAT3 by peptide hormone bradykinin (BK) in COS-7 cells. (aspetjournals.org)
  • These serious side effects have been attributed to bradykinin (a pro-inflammatory peptide and potent vasodilator) which has a short half-life that is rapidly inactivated in plasma by two exopeptidases, ACE and aminopeptidase P (APP). (ssc.ca)
  • Nous avons préalablement démontré que l'endothéline-1 (ET-1), un peptide vasoconstricteur de 21 acides aminés, joue un rôle central dans le métabolisme des tissus articulaires et a des fonctions cataboliques sur le cartilage articulaire dans l'ostéoarthrose, en liant son récepteur de type A (ETA). (umontreal.ca)
  • We describe the effects in isolated model sensory neurons of LAs on responses to the algogenic and sensitizing peptide, bradykinin (BK). (ovid.com)
  • Des-Pro2] Bradykinin Peptide inhibits angiotensins. (abbiotec.com)
  • Bradykinin is an inflammatory peptide that causes a local increase in vascular permeability. (uu.nl)
  • Bradykinin may mediate this via pro-inflammatory peptides (e.g. substance P, neuropeptide Y) and a local release of histamine. (wikipedia.org)
  • Bradykinins (BKs) belong to a family of short, structurally similar peptides that are important metabolites of the kallikrein-kinin system. (eurogentec.com)
  • Increasing evidence suggests that bradykinin is a member of a group of locally produced peptides which may act in a paracrine fashion as microenvironmental modulators of cell proliferation. (nih.gov)
  • Venom Bradykinin-Related Peptides (BRPs) and Its Multiple Biological Roles, An Integrated View of the Molecular Recognition and Toxinology Gandhi Rádis Baptista, IntechOpen, DOI: 10.5772/52872. (intechopen.com)
  • This implies that the synthesis of prostaglandins contributes to the bradykinin-evoked release of peptides. (jneurosci.org)
  • 3. Use according to either of the preceding claims, characterized in that the bradykinin antagonist is chosen from optionally modified, natural or synthetic peptides, natural or synthetic chemical molecules, antisense nucleic acids, ribozymes, anti-bradykinin antibodies, soluble bradykinin receptors, anti-bradykinin-receptor antibodies or bradykinin receptor antagonists. (freepatentsonline.com)
  • Figure 1: Bradykinin metabolism and its relationship with two other vasoactive mediators: angiotensin and natriuretic peptides. (kup.at)
  • The plasma concentration of the peptides bradykinin and des-Arg9-bradykinin was measured at different times that reflect equilibria between their formation and metabolism. (ssc.ca)
  • Bradykinin-related peptides, universal mediators of inflammation collectively referred to as the kinins, are often produced in excessive amounts during microbial infections. (uni-muenchen.de)
  • Bradykinins have been implicated in cell proliferation and migration in gastric cancers, and bradykinin antagonists have been investigated as anti-cancer agents. (wikipedia.org)
  • All of the clinically relevant effects of bradykinin appear to be mediated via the classical B 2 receptors and, wherever tested, were found to be reversible by B 2 receptor antagonists. (wipo.int)
  • Antagonists of bradykinin have been used to study various cardiovascular effects that bradykinin exerts, either directly or via interaction with other vasoactive substances, by assessing the effects of chronic B 2 receptor inhibition of bradykinin on systemic or regional hemodynamics, cardiac function and other vasoactive systems. (wipo.int)
  • One of the commonly used and most potent antagonists of bradykinin has the sequence: D-Arg-Arg-Pro-Hyp-Gly-Thi-Ser-D-Phe-Thi-Arg (D-Arg 0 , Hyp 3 , Thi 5 ' 8 , D-Phe 7 -BK). (wipo.int)
  • Bradykinin receptors and their antagonists. (alfa.com)
  • Bradykinin receptors antagonists and nitric oxide synthase inhibitors in vincristine and streptozotocin induced hyperalgesia in chemotherapy and diabetic neuropathy rat model. (nel.edu)
  • Therefore, concomitant administration of small doses of bradykinin receptor antagonists and NO synthase inhibitors can be effective in alleviation of neuropathic pain, even in hospital care. (nel.edu)
  • Guinea-pig tracheal smooth muscle cells were isolated and maintained in culture for 14-21 days prior to the study of the effect of a selective bradykinin B1 agonist and B2 antagonists upon bradykinin-stimulated phospholipase C and D activities. (strath.ac.uk)
  • Chemical cross-linking was used to analyze the binding sites for the agonist bradykinin (BK) and the antagonists NPC17731 and HOE140 on the bovine B2 bradykinin receptor. (lu.se)
  • It is thought that bradykinin is converted to inactive metabolites by ACE, therefore inhibition of this enzyme leads to increased levels of bradykinin, which causes a dry cough via bronchoconstriction. (wikipedia.org)
  • ACE Inhibition and Bradykinin-Mediated Renal Vascular Responses. (ahajournals.org)
  • B. S. McAllister, F. Leeb-Lundberg, and M. S. Olson, "Bradykinin inhibition of EGF- and PDGF-induced DNA synthesis in human fibroblasts," American Journal of Physiology , vol. 265, no. 2, pp. (hindawi.com)
  • Bradykinin-induced growth inhibition of normal rat kidney (NRK) cells is paralleled by a decrease in epidermal-growth-factor receptor expression," Biochemical Journal , vol. 298, no. 2, pp. 335-340, 1994. (hindawi.com)
  • In addition, the analogue RAP-L1, T6, L8-BK completely abolished these effects on selected rat smooth muscle tissues, whilst it showed inhibition effect on bradykinin-induced rat tail artery relaxation. (mdpi.com)
  • The analogue RAP-L1, T6, L8-BK further enhanced the bradykinin inhibitory activity only under the condition of co-administration with HOE140 on rat tail artery, suggesting a synergistic inhibition mechanism by which targeting B2 type receptors. (mdpi.com)
  • [7-10] Recently, Loeb and colleagues reported that halothane (0.5 mM, equal to 1.5 vol%), but not isoflurane, selectively inhibits bradykinin-induced calcium currents and prostacyclin production in vitro in cultured bovine aortic endothelial cells, and that inhibition of prostacyclin release may result in the decreased vasodilation observed with halothane versus isoflurane. (asahq.org)
  • Inhibition of bradykinin abolished the effect of captopril on the lower limit of CBF autoregulation. (ahajournals.org)
  • The bradykinin-induced inhibition of the amplitude of the [Ca2+]i transient was more pronounced at shorter voltage steps. (aspetjournals.org)
  • The results of this paper confirm that inhibition of bradykinin receptors and inducible NO synthase but not neuronal NO synthase activity reduces diabetic hyperalgesia. (nel.edu)
  • Although astrocytes stimulated with bradykinin did not undergo cell swelling, the bradykinin‐activated current exhibited properties typical of VSOR: outward rectification, inhibition by osmotic shrinkage, sensitivity to DIDS, phloretin and DCPIB, dependence on intracellular ATP, and permeability to glutamate. (deepdyve.com)
  • Inhibition of both aminopeptidase P and angiotensin-converting enzyme prevents bradykinin degradation in the rat coronary circulation. (semanticscholar.org)
  • Inhibition of aminopeptidase P potentiates wheal response to bradykinin in angiotensin-converting enzyme inhibitor-treated humans. (semanticscholar.org)
  • Although ACE inhibitors increase bradykinin concentrations in addition to their effect on angiotensin II formation, the role of bradykinin in renal fibrosis has not been studied. (jci.org)
  • The sole role of bradykinin (BK) as an inflammatory mediator is controversial, as recent data also support an anti-inflammatory role for BK in Alzheimer's disease (AD). (rsc.org)
  • Haemorrhage is associated with the endogenous release of bradykinin, which may subsequently stimulate the formation of nitric oxide (NO). The present study investigated the relative contribution of NO synthase (NOS) isoforms and the role of bradykinin in the pathogenesis of splanchnic hyposensitivity to a long-acting vasopressin analogue, glypressin, in rats with portal hypertension induced by partial portal vein ligation (PVL). (clinsci.org)
  • The bradykinin potentiators, which possess no bradykinin activity themselves, enhance the activity of bradykinin. (fishersci.ca)
  • In streptozotocin-induced hyperalgesia, inducible NO synthase participates in pronociceptive activity of bradykinin, whereas in vincristine-induced hyperalgesia bradykinin seemed to activate neuronal NO synthase pathway. (nel.edu)
  • While mast cell -mediated angioedema can be successfully treated with antihistamines and glucocorticosteroids and with omalizumab as a prophylactic treatment [ 6 ], Bk-AE requires interventions that target the synthesis or receptor activity of bradykinin. (biomedcentral.com)
  • In this experiment, we studied the effect of bradykinin on noradrenaline spillover in the in situ canine gracilis muscle, using the specific B 2 antagonist HOE 140. (ingentaconnect.com)
  • HOE 140 (a bradykinin B2 receptor antagonist) was started in the operating room after induction of anesthesia and before heparinization, continued throughout the bypass period, and discontinued at the end of surgery. (clinicaltrials.gov)
  • n is used as a bradykinin-1 receptor (B1R) antagonist frequently in comparison with the B1 receptor agonist des-Arg9-bradykinin. (sigmaaldrich.com)
  • Hypertensive effect of a bradykinin antagonist in normotensive rats. (ahajournals.org)
  • The bradykinin analogue B4146, a competitive antagonist-partial agonist of bradykinin, was used in three groups of normotensive unanesthetized Wistar rats. (ahajournals.org)
  • The bradykinin antagonist produced an average increase in mean arterial pressure of approximately 13 mm Hg for all groups. (ahajournals.org)
  • Since smaller doses of B4146, sufficient to block exogenous bradykinin, do not cause changes in normal blood pressure, we conclude that endogenous bradykinin does contribute to normal blood pressure maintenance, but its effect can be demonstrated only if very high doses of its antagonist are injected, maybe because a high concentration of the compound is necessary to displace not only circulating but possibly tissue receptor-bound bradykinin as well. (ahajournals.org)
  • Classical agonist of this receptor includes bradykinin1-8 (bradykinin with the first 8 amino acid) and antagonist includes [Leu8]-bradykinin1-8. (wikidoc.org)
  • The use of an effective amount of at least one bradykinin antagonist as the active principle in a physiologically acceptable medium in a cosmetic composition or for preparing a drug is disclosed. (freepatentsonline.com)
  • 1. Use, in a cosmetic composition or for the preparation of a medicinal product, of an effective amount of at least one bradykinin antagonist, this antagonist or the medicinal product being intended to induce and/or stimulate hair growth and/or slow down hair loss. (freepatentsonline.com)
  • 2. Use according to the preceding claim, characterized in that the bradykinin antagonist is chosen from compounds which inhibit the synthesis and/or accelerate the catabolism of bradykinin, bradykinin neutralizers, bradykinin receptor blockers such as those which interfere with the effects of bradykinin by binding to its receptor (B1 or B2), compounds which inhibit the synthesis of bradykinin receptors or compounds involved in modulating the signal transduced by bradykinin. (freepatentsonline.com)
  • 4. Use according to any one of the preceding claims, characterized in that the bradykinin antagonist is chosen from compounds which interfere with the effects of bradykinin by binding to its receptor (B1 or B2) and preferably to the B2 receptor. (freepatentsonline.com)
  • 6. Use according to the preceding claim, characterized in that the bradykinin antagonist is D-Arg, [Hyp3, Thi5, D-Tic7, Oic8]bradykinin (HOE 140). (freepatentsonline.com)
  • 0001] The present invention relates to the use, as active principle, in a physiologically acceptable medium, in a cosmetic composition or for the preparation of a medicinal product, of an effective amount of at least one bradykinin antagonist which is intended to induce and/or stimulate hair growth and/or slow down hair loss. (freepatentsonline.com)
  • By using canonical antagonist for bradykinin B1 or B2 type receptors, we found that RAP-L1, T6-BK -induced relaxation of the arterial smooth muscle was very likely to be modulated by B2 receptors. (mdpi.com)
  • Systemic infusion of bradykinin receptor antagonist (HOE-140). (clinicaltrials.gov)
  • The B- receptors are sensitive to the bradykinin metabolite des-Arg 9 -BK, and B 1 -mediated effects are blocked by the specific antagonist des-Arg 9 -Leu 8 -BK. (wipo.int)
  • To investigate the role of endogenously produced bradykinin in modulating renal function during postnatal maturation, various parameters of glomerular and tubular function were measured for 1 h before and after intravenous injection of 12.5 μg/kg of the specific B 2 -receptor antagonist icatibant to conscious, chronically instrumented lambs aged ∼1 ( n = 7) and ∼6 wk ( n = 7). (physiology.org)
  • To evaluate contrast-enhanced ultrasound (CE-US) as a monitoring tool to assess hypervascularisation of synovial processes in knee osteoarthritis (OA) treated with intra-articular injections of the bradykinin-receptor 2 antagonist icatibant compared to contrast-enhanced magnetic resonance imaging (CE-MRI). (bmj.com)
  • a non-selective NOS inhibitor), L -canavanine (a specific inhibitor of inducible NOS) or HOE 140 (a bradykinin B 2 receptor antagonist) was administered 45 min before the infusion of glypressin. (clinsci.org)
  • However, bradykinin-stimulated (10 nM, EC100) [3H]-PtdBut accumulation was poorly inhibited and with low potency by each B2 receptor antagonist and bradykinin-stimulated phospholipase D activity persisted at concentrations of antagonist that completely blocked bradykinin-stimulated Ins(1,4,5)P3 formation (30 microM). (strath.ac.uk)
  • Bradykinin activates sphingolipid metabolism. (fishersci.ca)
  • In severe cases, the elevation of bradykinin may result in angioedema , a medical emergency. (wikipedia.org)
  • Overactivation of bradykinin is thought to play a role in a rare disease called hereditary angioedema , formerly known as hereditary angio-neurotic edema. (wikipedia.org)
  • Increased levels of bradykinin, which can cause swelling, may contribute to the development of angioedema. (clinicaltrials.gov)
  • Blocking bradykinin receptor cells prevents bradykinin from initiating swelling and may lead to a possible decrease in angioedema symptoms. (clinicaltrials.gov)
  • The purpose of this study is to evaluate the effectiveness of HOE-140, a bradykinin receptor blocker, at reducing symptoms in people with ACE inhibitor-associated angioedema. (clinicaltrials.gov)
  • Bradykinin mediated angioedema in patient using angiotensin-converting enzyme inhibitors (ACEI) presented with. (srce.hr)
  • Bradykinin mediated angioedema,including hereditary and ACEI induced forms,does not respond to conventional antihistamine and corticosteroid therapy. (srce.hr)
  • We have learned from patients with the disease hereditary angioedema that uncontrolled bradykinin production leads to episodes with swelling of submucosal and subcutaneous tissue. (uu.nl)
  • We developed an assay to detect bradykinin release and demonstrated its use as compound diagnostic in drug development for hereditary angioedema. (uu.nl)
  • We found evidence for increased bradykinin production in patients with chronic spontaneous urticaria and started a pilot study looking for novel treatment options for patients with idiopathic angioedema. (uu.nl)
  • Bradykinin-mediated angioedema (Bk-AE) can be life-threatening and requires specific targeted therapies. (biomedcentral.com)
  • Angioedema is a swelling of the deeper layers of the skin and mucous membranes subsequent to blood vessel dilation and increased vascular permeability induced by vasoactive mediators such as histamine and bradykinin. (biomedcentral.com)
  • COLLIER H.O.J., JAMES G.W.L. and PIPER P.J. (1965) - Intensifica tion by adrenalectomy or by 8-adrenergic blockade of the bronchoconstrictor action of bradykinin in the guinea-pig. (springer.com)
  • Localization of central pressor action of bradykinin in medulla oblongata. (biomedsearch.com)
  • Effect of histamine and bradykinin on lymph and tissue fluid composition in the rabbit hindlimb: evidence for two compartments in tissue fluid. (biomedsearch.com)
  • To investigate the effect of Tongluotangtai decoction on 5-HT, β-EP, histamine and bradykinin in serum of STZ rats with pain-related diabetic neuropathy. (alliedacademies.org)
  • The rats were administrated with saline, Tongluo sugar Thai or phenytoin sodium daily, and the levels of 5- HT, β-EP, histamine and bradykinin in the serum of each group were measured after 3 w, 5 w and 9 w. (alliedacademies.org)
  • Compared with the model group, the contents of histamine and bradykinin in Tongtao Tangtai group and phenytoin group were significantly decreased and the level of β-EP was significantly reduced. (alliedacademies.org)
  • Tongtao Tangtai decoction can significantly reduce the level of 5-HT, histamine and bradykinin in STZ-induced diabetic neuropathy model rats, increase the content of β-EP and exert a significant anti-pain effect. (alliedacademies.org)
  • Bradykinin dilates blood vessels via the release of prostacyclin , nitric oxide , and Endothelium-Derived Hyperpolarizing Factor . (wikipedia.org)
  • BACKGROUND: This study investigates bradykinin and nitric oxide as potential mediators of AT2-receptor-stimulated duodenal mucosal alkaline secretion. (gu.se)
  • Bradykinin also contracts smooth muscles and is a potent stimulator of nitric oxide formation by vascular endothelium. (eurogentec.com)
  • Bradykinin is a potent vasodilator that acts through endothelial B2 kinin receptors to stimulate the release of nitric oxide and endothelium-derived hyperpolarizing factor. (hmdb.ca)
  • Bradykinin, a mediator of hypersensitivity, is also a potent coronary vasodilator, acting via nitric oxide and prostacyclin production. (ahajournals.org)
  • We postulate that bradykinin plays a protective role in cardiac anaphylaxis by accumulating at the luminal surface of the coronary endothelium and promoting, in an autocrine mode, a B 2 -receptor-mediated production of nitric oxide and prostacyclin in concentrations sufficient to elicit a paracrine effect on coronary vascular smooth muscle, thus opposing the vasoconstricting effects of other anaphylactic mediators. (ahajournals.org)
  • Bradykinin has long been known as a potent coronary vasodilator, 7 and its action is mediated by endothelium-derived mediators, such as prostacyclin (PGI 2 ) and nitric oxide. (ahajournals.org)
  • Bradykinin is a vasoactive kinin that is liberated from its substrate kininogen by the action of kallikrein, and is known to be involved in a wide range of biologic processes. (hmdb.ca)
  • Bradykinin (BK) is a vasoactive nonapeptide released from kininogens by the proteolytic activity of kallikreins. (aspetjournals.org)
  • A class of drugs called ACE inhibitors , which are used to lower blood pressure, increase bradykinin (by inhibiting its degradation), further lowering blood pressure. (wikipedia.org)
  • A class of drugs called angiotensin converting enzyme inhibitors (ACE inhibitors) increase bradykinin levels by inhibiting its degradation, thereby increasing its blood pressure lowering effect. (wikipedia.org)
  • These imbalances cause bradykinin levels to increase - in fact, most of the proteins involved in bradykinin production and signaling are undetectable in such lung fluid under normal conditions, but go up sharply during coronavirus infection, while enzymes that are involved in bradykinin degradation go down. (sciencemag.org)
  • As with bradykinin, the enzymes involved in its production are all ramped up rather steeply in the coronavirus patient samples, and the ones involved in its degradation are all down. (sciencemag.org)
  • The increased interstitial fibrosis in B2 -/- mice was accompanied by a decreased activity of plasminogen activators (PAs) and metalloproteinase-2 (MMP-2), enzymes involved in ECM degradation, suggesting that the protective effects of bradykinin involve activation of a B2 receptor/PA/MMP-2 cascade. (jci.org)
  • ACEI inhibit bradykinin degradation because angiotensin II is a key factor for the inactivation of bradykinin. (srce.hr)
  • Bradykinin is used to lower blood pressure, increase bradykinin (by inhibiting its degradation) further lowering blood pressure. (alfa.com)
  • The renin-angiotensin and kininogen-kinin hormonal systems are critically involved in regulating blood pressure and are candidates in contributing to oral contraceptive pill (OCP)-induced hypertension.Angiotensin-converting enzyme (ACE) and aminopeptidase P (AP-P) are key enzymes in these systems and are both involved in the degradation of the vasodilator bradykinin. (semanticscholar.org)
  • ACE is critical in the degradation of bradykinin, which is hypothesized to accumulate excessively in some patients taking ACEI for their hypertension. (biomedcentral.com)
  • Bradykinin-induced Ca 2+ increase in cells is mediated by the stimulation of kinin receptors of the B2 subtype. (eurogentec.com)
  • The purified SAP2 was shown to cleave human kininogens, preferably the low molecular mass form (LK) and optimally in an acidic environment (pH 3.5-4.0), and to produce two kinins, Met-Lys-bradykinin and its derivative, {[}Hydroxyproline(3)]-Met-Lys-bradykinin, both of which are capable of interacting with cellular bradykinin receptors of the B2 subtype. (uni-muenchen.de)
  • Bradykinin is also thought to be the cause of the dry cough in some patients on widely prescribed angiotensin-converting enzyme (ACE) inhibitor drugs. (wikipedia.org)
  • Increased levels of bradykinins resulting from ACE inhibitor use have been associated with increased lung cancer risks. (wikipedia.org)
  • This agent elicits specific kallikrein inhibitor activity resulting in bradykinin reduction. (medscape.com)
  • Hence, we investigated whether the effect of an ACE inhibitor on the lower limit of CBF autoregulation is mediated by the potentiation of bradykinin-mediated vasodilatation. (ahajournals.org)
  • The aim here was to evaluate the response to therapy for these attacks using icatibant, an inhibitor of the bradykinin receptor, which was recently introduced into Brazil. (scielo.br)
  • Pretreatment of mouse astrocytes with either a ROS scavenger or an NAD(P)H oxidase inhibitor blocked bradykinin‐induced activation of VSOR, glutamate release and astrocyte‐to‐neuron signalling. (deepdyve.com)
  • Uncontrolled generation of bradykinin, on the other hand, occurs when complement-1 inhibitor (C1-INH) is either deficient or non-functioning. (biomedcentral.com)
  • We show here that genetic ablation ( B2 -/- mice) or pharmacological blockade of the bradykinin B2 receptor increases UUO-induced interstitial fibrosis in mice, whereas transgenic rats expressing increased endogenous bradykinin show reduced UUO-induced interstitial fibrosis. (jci.org)
  • In sample of plasma from each patient, concentrations of endogenous bradykinin produced by kinin-forming activitation in plasma during a period of 60 minutes were measured in vitro using a physical chemical technique. (ssc.ca)
  • The subsequent release of the nonapeptide vasodilator bradykinin (BK) in the joint microenvironment, and up-regulation of bradykinin receptor B1 (BKB1) expression, engenders a vicious cycle of synovial membrane inflammation, articular cartilage destruction, and joint pain. (umontreal.ca)
  • Bradykinin is an inflammatory mediator . (wikipedia.org)
  • Several Authors have demonstrated the occurrence of bradykinin in tissues affected by allergic and inflammatory processes: this find ing allowed them to postulate the participation of the polypeptide in the pathologic alterations of the vascular permeability and of the smooth muscle motility (Rocha e Silva, 1970). (springer.com)
  • Prostaglandins are known to enhance the inflammatory and nociceptive actions of other chemical mediators of inflammation such as bradykinin. (jneurosci.org)
  • The augmentation of bradykinin-induced release of iSP and iCGRP by PGE2 may be one mechanism to account for the inflammatory and hyperalgesic actions of this eicosanoid. (jneurosci.org)
  • The aim of this study is to assess how clot forming and clot dissolving pathways are affected during this process, and examine the role of a natural inflammatory hormone, bradykinin. (clinicaltrials.gov)
  • pain and myocardial reperfusion arrhythmias, bronchial asthma and allergic rhinitis, toxic shock and circulatory collapse, orthostatic hypotension and possibly other B 2 mediated effects of bradykinin that are still ill-defined, such as pain, bowel hypermobility and diarrhea of chronic inflammatory intestinal disease, painful arthritis, neuralgia, etc. (wipo.int)
  • After intravenous administration of Evans blue dye, we perfused normal saline followed by bradykinin or platelet-activating factor, another inflammatory mediator, intraarticularly via needles placed in the knee joint. (asahq.org)
  • [2-6] A few of these reports studied volatile anesthetic effects on the vasomotor actions of bradykinin, serotonin, and other inflammatory mediators. (asahq.org)
  • [5,11] However, bradykinin-induced prostanoid release is also important in local inflammatory processes. (asahq.org)
  • Bradykinin (BK) is a nonapeptide that contributes to inflammatory responses, mediates pain signals and influences blood pressure. (diva-portal.org)
  • Intracellular INK pathway and TNF-alpha might provide key links between inflammatory mediators like IL-1 beta and airway hyperresponsiveness to bradykinin. (lu.se)
  • To evaluate the hypothesis that sphingosine-1-phosphate (S1P) and cAMP attenuate increased permeability of individually perfused mesenteric microvessels through a common Rac1-dependent pathway, we measured the attenuation of the peak hydraulic conductivity (L p ) in response to the inflammatory agent bradykinin (BK) by either S1P or cAMP. (elsevier.com)
  • A September 1, 2020, Medium article 1 by Thomas Smith reviewed the findings of what is now referred to as the bradykinin hypothesis. (mercola.com)
  • The bradykinin hypothesis provides a model that helps explain some of the more unusual symptoms of COVID-19, including its bizarre effects on the cardiovascular system. (mercola.com)
  • This is the "bradykinin hypothesis", and before digging into it, it might be worth a paragraph to talk about what bradykinin is. (sciencemag.org)
  • The hypothesis is presented diat bradykinin is produced from kininogen in the lungs of the fetal lamb when oxygenated, and that the maximal rate of production occurs during the first few minutes after expansion of the lungs or exposure of the ewe and fetus to hyperbaric O 2 . (ahajournals.org)
  • Expression of bradykinin receptors in the left ventricles of rats with pressure overload hypertrophy and heart failure," Journal of Hypertension , vol. 21, no. 9, pp. 1729-1736, 2003. (hindawi.com)
  • Bradykinin injected into the fourth cerebral ventricle of unanesthetized rats produced a pressor effect with a shorter latency and a larger maximal effect than when injected in the third or lateral ventricles. (biomedsearch.com)
  • Montana and Sontheimer also learned that bradykinin acts as a chemoattractant, guiding glioma cells toward blood vessels in the brains of rats. (oncologynurseadvisor.com)
  • Results: Bradykinin increased plasma extravasation eight- to ninefold above baseline in both pentobarbital- and isoflurane-anesthetized rats. (asahq.org)
  • The kinin-kallikrein system makes bradykinin by proteolytic cleavage of its kininogen precursor, high-molecular-weight kininogen (HMWK or HK), by the enzyme kallikrein . (wikipedia.org)
  • the conversion of kininogen to bradykinin, which is also a powerful vasodilator. (britannica.com)
  • Bradykinin is released from kininogen by plasma kallikrein. (abcam.com)
  • Furthermore, bradykinin is a likely mediator of immediate hypersensitivity, because circulating levels of high molecular weight kininogen, a precursor of bradykinin, decrease during anaphylactic shock in humans. (ahajournals.org)
  • lysyl-bradykinin, a kinin produced by the action of tissue and glandular kallikreins on low-molecular-weight kininogen and having physiologic effects similar to those of bradykinin. (thefreedictionary.com)
  • The present study showed that bradykinin precursor, kininogen, is present in arterial blood of the fetal lamb by 61 days of gestation and that its concentration increases toward term. (ahajournals.org)
  • Kininogen concentrations in left atrial blood decreased within 1 to 2 minutes after beginning ventilation with O 2 , and free bradykinin was detected in left atrial blood. (ahajournals.org)
  • Associated with a mean increase in brachial arterial blood Po 2 to 44 mm Hg, a value equivalent to that in the ventilated exteriorized fetus, kininogen concentration fell, and free bradykinin was detected in the brachial arterial blood of 3 of the 6 fetuses. (ahajournals.org)
  • bradykinin, for example, causes contraction of most smooth muscles and has a very potent action in dilating certain blood vessels. (britannica.com)
  • Bradykinin is inactivated by a kininase, which also converts angiotensin I to angiotensin II, a substance that causes the constriction of blood vessels. (britannica.com)
  • Bradykinin lowers blood pressure by dilating blood vessels, but it causes contraction of the smooth muscle in the lungs and in the gut. (sciencemag.org)
  • This interfered with the receptor's ability to bind to bradykinin and lead the cells to nourishing blood vessels. (oncologynurseadvisor.com)
  • These data strongly suggest that bradykinin, acting via B2R, acts as an important signal directing the invasion of glioma cells toward blood vessels," concluded Montana and Sontheimer in their paper. (oncologynurseadvisor.com)
  • Previous studies have shown that bradykinin induces pain and causes blood vessels to expand and become leaky which will lead to swelling and inflammation of the surrounding tissue. (elifesciences.org)
  • Western blotting revealed the presence of Gq/G11 which couples to the inositol lipid-directed phospholipase C. Indomethacin (10 microM) was without effect upon bradykinin-stimulated phospholipase D activity, suggesting that the bradykinin effects were not mediated indirectly by cyclooxygenase products. (strath.ac.uk)
  • Accordingly, we postulate that bradykinin is a protective mediator of cardiac anaphylaxis. (ahajournals.org)
  • Since bradykinin is an initial mediator of inflammation, VSOR might play a role in glia-neuron communication in the brain during inflammation. (deepdyve.com)
  • Bradykinin has multiple physiological effects such as smooth muscle contraction, hypotension induction, natriuresis and diuresis, decrease in blood glucose level, inflammation mediator, and increase of vascular permeability. (abbiotec.com)
  • Bradykinin receptors (there are two types ) can signal to attract neutrophils (giving it a role in allergy and inflammation), and its pathways have also shown up in the functioning of several types of cancer cells. (sciencemag.org)
  • Conclusion: Halothane, but not isoflurane or pentobarbital, inhibits both baseline and bradykinin-induced peripheral plasma extravasation, demonstrating that volatile anesthetics differentially modulate this important component of inflammation. (asahq.org)
  • Bradykinin acts through two receptor subtypes in mammals and generates a variety of responses including pain, inflammation and hypotension. (diva-portal.org)
  • We have previously demonstrated, using a murine in vitro model of chronic airway inflammation, that TNF-alpha up-regulated bradykinin B-1 and B-2 receptors in the airway smooth muscle. (lu.se)
  • Bradykinin receptor B1 (B1) is a G-protein coupled receptor encoded by the BDKRB1 gene in humans. (wikipedia.org)
  • We offer Bradykinin RB1/BDKRB1 Lysates for use in common research applications: Western Blot. (novusbio.com)
  • Each Bradykinin RB1/BDKRB1 Lysate is fully covered by our Guarantee+, to give you complete peace of mind and the support when you need it. (novusbio.com)
  • Our Bradykinin RB1/BDKRB1 Lysates can be used in a variety of model species: Human. (novusbio.com)
  • Choose from our Bradykinin RB1/BDKRB1 Lysates. (novusbio.com)
  • To explore the role of the kallikrein-kinin system in relation to ischemia/reperfusion injury in the kidney, we generated mice lacking both the bradykinin B1 and B2 receptor genes (B1RB2R-null, Bdkrb1-/-/Bdkrb2-/-) by deleting the genomic region encoding the two receptors. (nih.gov)
  • Bradykinin plays an important role in the regulation of fluid and electrolyte balance, smooth muscle contraction, vasodilation and capillary permeability. (fishersci.ca)
  • alpha-Thrombin, bradykinin, and histamine are endogenous mediators that increase endothelial permeability. (nih.gov)
  • Addition of alpha-thrombin, bradykinin, or histamine increased the permeability coefficient of the HUVEC monolayer. (nih.gov)
  • alpha-Thrombin and bradykinin induced HUVEC permeability was increased for the first 90 min after which it returned to control levels. (nih.gov)
  • These data also show, for the first time, that histamine and alpha-thrombin increased permeability by calcium-dependent intracellular pathways, but bradykinin operates through a calcium-independent mechanism. (nih.gov)
  • Bradykinin caused platelet adhesion on the apparently unbroken endothelium of the femoral vein, decreased peripheral vascular resistance of the microcirculation and increased permeability of venules of the vasa vasorum of the abdominal aorta in dogs. (ebscohost.com)
  • Bradykinin is a very potent vasodilator and increases permeability of post capillary venules , it acts on endothelial cells to activate phospholipase A2. (biology-online.org)
  • Kinins exert multiple pathophysiological functions, including vascular permeability and mitogenesis, by activating their cognate receptors, bradykinin subtype 1 receptor (B1R) and bradykinin subtype 2 receptor (B2R), which belong to the superfamily of G protein-coupled receptors. (aacrjournals.org)
  • This very atypical pattern of the RAS is predicted to elevate bradykinin levels in multiple tissues and systems that will likely cause increases in vascular dilation, vascular permeability and hypotension. (elifesciences.org)
  • The bradykinin receptor family is a group of G-protein coupled receptors whose principal ligand is the protein bradykinin. (wikipedia.org)
  • The B1 receptor is one of two G protein-coupled receptors that have been found which bind bradykinin and mediate responses to these pathophysiologic conditions. (wikipedia.org)
  • And the bradykinin B2 receptor forms an actual protein complex with angiotensin-converting enzyme itself, although all the functions behind this haven't been worked out. (sciencemag.org)
  • It directly activates afferent neurons via G protein-coupled bradykinin B2 receptors. (eurogentec.com)
  • The translocation with bradykinin occurred even after pretreatment with an islet-activating protein, wortmannin, and phorbol 12,13-dibutyrate. (diabetesjournals.org)
  • The bradykinin and neuropeptide Y (NPY) receptors belong to the superfamily of G-protein coupled receptors (GPCRs). (diva-portal.org)
  • Lymphatic protein and LDH fluxes were increased both by bradykinin and histamine. (biomedsearch.com)
  • Bradykinin raises internal calcium levels in neocortical astrocytes causing them to release glutamate , though this finding has only been confirmed in-vitro. (wikipedia.org)
  • Maximum intracellular calcium in HUVEC was increased by alpha-thrombin (245 +/- 20 nM) and histamine (210 +/- 22 nM), but not by bradykinin (70 +/- 7 nM) as compared to control (69 +/- 10). (nih.gov)
  • Bradykinin inhibits a calcium-dependent potassium current responsible for an afterspike hyperpolarization in nodose ganglion. (eurogentec.com)
  • Bradykinin alone causes a concentration-dependent increase in the release of iSP and iCGRP from isolated sensory neurons, and this action is abolished in the absence of extracellular calcium. (jneurosci.org)
  • Chad, J.E. and Yeats, J.C. (1986) Calcium fluxes activated during neurite spiking induced by bradykinin. (soton.ac.uk)
  • Bradykinin-induced modulation of calcium signals in rat dorsal root ganglion neurons in vitro. (aspetjournals.org)
  • The reduction in [Ca2+]i produced by bradykinin in sensory neurons may be an important factor contributing to bradykinin-induced excitation of primary sensory afferents. (aspetjournals.org)
  • To determine whether cold could activate the kallikrein-kinin system in vivo as it does in vitro, the circulating systemic concentrations of bradykinin were serially measured in 10 cyildren with congenital diseases of the heart undergoing corrective cardiac surgery. (ahajournals.org)
  • 8 Local bradykinin production can occur in the heart by an independent kallikrein-kinin system present in the coronary vessels. (ahajournals.org)
  • On the other hand, ACE inhibitors are capable of inactivating kininase II, a kinin-degrading enzyme, which would result in accumulation of bradykinin. (ahajournals.org)
  • Bradykinin (BK) stimulates B2 kinin receptors to activate multiple signaling pathways in trabecular meshwork (TM) cells. (arvojournals.org)
  • These observations suggest that the activation of phospholipase C by bradykinin may be mediated through a bradykinin B2 receptor population, whereas bradykinin-stimulated phospholipase D may be activated via a distinct population of bradykinin receptors that do not appear to be either B1 or B2 receptor types, based upon pharmacological specificity. (strath.ac.uk)
  • The bradykinin BK2 receptor mediates angiotensin II receptor type 2 stimulated rat duodenal mucosal alkaline secretion. (gu.se)
  • Under physiological conditions, the bradykinin B2 (BKB2) receptor is constitutively expressed and mediates most of kinins' actions. (aspetjournals.org)
  • Studies have demonstrated that bradykinin, through the B2 bradykinin receptor (B2BKR), mediates important cardiovascular effects that may protect against LV hypertrophy. (diva-portal.org)
  • Most of the physiological responses to bradykinin appear to be mediated through activation of the B 2 receptor, which is the most prevalent receptor subtype within the body. (physiology.org)
  • The circulating concentrations of bradykinin increased significantly as body temperature decreased during surface cooling. (ahajournals.org)
  • With the onset of cardiopulmonary bypass and hence, removal of the lung and pulmonary converting enzyme from the circulation, there was a further rise in the already elevated concentrations of bradykinin. (ahajournals.org)
  • This is the first in vivo demonstration that hypothermia leads to an increase in the circulating concentrations of bradykinin. (ahajournals.org)
  • Bradykinin is a polypeptide that circulates in the plasma in very low concentrations in comparison with the amount of bradykinin found in various body tissues. (hmdb.ca)
  • Study the relationships of the profiles for bradykinin and des-Arg9-bradykinin with gender and the concentrations of angiotensin I-converting enzyme, aminopeptidase P, and carboxypeptidase N. (ssc.ca)
  • A bradykinin-potentiating factor (BPF) which increases both the duration and magnitude of the effects of bradykinin on vasodilation and the consequent fall in blood pressure, was discovered in Bothrops jararaca venom. (wikipedia.org)
  • However, previous experiments in mice and computer simulations indicate that modest increases in angiotensin-converting enzyme have minimal effects on blood pressure and angiotensin II levels, although bradykinin decreases significantly, inferring that bradykinin is critical for protecting the kidney in diabetics. (pnas.org)
  • Bradykinin production in the lung increases with many pulmonary diseases such as asthma, bronchitis, and pneumonia. (eurogentec.com)
  • Thus, absence of the bradykinin B2 receptor increases the oxidative stress, mitochondrial DNA damage, and many senescence-associated phenotypes already present in untreated Akita diabetic mice. (jci.org)
  • Because ischemia increases bradykinin outflow from the heart, we questioned whether bradykinin might mitigate anaphylactic coronary vasoconstriction. (ahajournals.org)
  • 9 Myocardial ischemia increases bradykinin outflow from the heart, 10 11 an effect that is potentiated by kininase II/angiotensin-converting enzyme (ACE) inhibitors 11 and is viewed as cardioprotective. (ahajournals.org)
  • 13 Because cardiac anaphylaxis is associated with marked ischemia caused by an array of coronary-vasoconstricting agents 1 and ischemia increases bradykinin outflow from the heart, 10 we questioned whether bradykinin production is increased during cardiac anaphylaxis and, if so, whether this nonapeptide may function as a mitigating factor against threatening vasoconstricting mediators. (ahajournals.org)
  • Comparison with BALF from controls identifies a critical imbalance in RAS represented by decreased expression of ACE in combination with increases in ACE2, renin, angiotensin, key RAS receptors, kinogen and many kallikrein enzymes that activate it, and both bradykinin receptors. (elifesciences.org)
  • To test this inference, we have combined the following two mutations: a dominant mutation that leads to maturity onset diabetes, Akita ( 7 ), resulting from an amino acid change in the insulin 2 gene ( Ins2 C96Y ) ( 8 ), and a recessive knockout mutation ( Bdkrb2 - ) ( 9 ) in the gene coding for the bradykinin B2 receptor, the receptor predominantly expressed in the normal kidney. (pnas.org)
  • In addition, silencing αCGRP gene expression, but not substance P, drastically reduced bradykinin-induced TRPV1 sensitization in peptidergic nociceptors. (frontiersin.org)
  • Promoter polymorphism of the β 2 bradykinin receptor gene is associated with essential hypertension," Japanese Circulation Journal , vol. 63, no. 10, pp. 759-762, 1999. (hindawi.com)
  • B. Wang, A. Dang, and G. Liu, "Genetic variation in the promoter region of the β 2 bradykinin receptor gene is associated with essential hypertension in a Chinese Han population," Hypertension Research , vol. 24, no. 3, pp. 299-302, 2001. (hindawi.com)
  • Lack of association of a 9 bp insertion/deletion polymorphism within the bradykinin 2 receptor gene with myocardial infarction," Clinical Science , vol. 107, no. 5, pp. 505-511, 2004. (hindawi.com)
  • Also the bradykinin precursor gene was identified in all of these species in a chromosome region with conserved synteny. (diva-portal.org)
  • For example, bradykinin synthesis and B 2 -receptor gene expression are activated in the developing rat kidney ( 7 , 8 ). (physiology.org)
  • GJURIS V., HEICKE B. and WESTERMANN E. (1964) - Uber die Stimulie rung der Atmung durch Bradykinin und Kallidin - Arch. (springer.com)
  • bradykinin was called kallidin I or 9 and lysyl-bradykinin was called kallidin II or 10. (thefreedictionary.com)
  • We found that bradykinin notably enhances the excitability of peptidergic nociceptors, and sensitizes TRPV1, primarily through the bradykinin receptor 2 pathway. (frontiersin.org)
  • Bradykinin directly triggers GLUT4 translocation via an insulin-independent pathway. (diabetesjournals.org)
  • Thus, VSOR activated by ROS in mouse astrocytes in response to stimulation with bradykinin, serves as the pathway for glutamate release to mediate astrocyte‐to‐neuron signalling. (deepdyve.com)
  • Removal of extracellular Ca2+ markedly reduced the bradykinin-stimulated phospholipase D response (by 73 +/- 10%, N = 3 experiments) but had only a limited effect upon PMA-stimulated phospholipase D activity (by 23 +/- 6%, N = 3 experiments). (strath.ac.uk)
  • Enkephalin activates the phospholipase C/Ca2+ system through cross-talk between opioid receptors and P2-purinergic or bradykinin receptors in NG 108-15 cells. (biochemj.org)
  • Thus EK can induce phospholipase C activation and subsequent Ca2+ mobilization, provided that the cells have been previously or are simultaneously stimulated by endogenous adenine nucleotides or by externally applied P2-agonists or bradykinin. (biochemj.org)
  • The bradykinin B1 agonist, desArg9-bradykinin (1 microM) was without effect upon phospholipase C or phospholipase D activity. (strath.ac.uk)
  • The mechanism of the activation of phospholipase D by bradykinin and the role of the putative B3 bradykinin receptor are discussed. (strath.ac.uk)
  • Their research shows that glioma cells isolated from patient biopsies express bradykinin 2 receptors (B2R), and that bradykinin significantly enhances glioma cell migration and invasion. (oncologynurseadvisor.com)
  • The amino acid sequence of bradykinin is: Arg-Pro-Pro-Gly-Phe-Ser-Pro-Phe-Arg (RPPGFSPFR). (wikipedia.org)
  • A decapeptide vasodilator consisting of bradykinin with a lysyl group attached to the amino terminus. (thefreedictionary.com)
  • These analogs generally have modifications or additions to one or more of the nine bradykinin amino acids. (wipo.int)
  • In one approach, the effect of bradykinin was studied by blocking its action via antibodies. (wipo.int)
  • Hydroxylation of Pro-383 occurs prior to the release of bradykinin. (abcam.com)
  • We found that bradykinin directly triggered GLUT4myc translocation and increased the rate of glucose uptake in a dose-dependent manner in these cells. (diabetesjournals.org)
  • IL-1 beta up-regulated bradykinin B-1 and B2 receptor expression and increased contractile response to bradykinin B-1 and B-2 receptor agonists (des-Argl-bradykinin and bradykinin, respectively) in the tracheal smooth muscle. (lu.se)
  • The data suggest that bradykinin may play a regulatory role in the central control of blood pressure by stimulating sites that are near the dorsal and dorsal lateral surfaces of the medulla and accessible to kinins in cerebrospinal fluid and in the cerebral arterial circulation. (biomedsearch.com)
  • LIM R.K.S., LIU C.N., GUZMAN F. and BRAUN C. (1962) - Visceral receptors concerned in visceral pain and the pseudo-affecti ve response to intra-arterial injection of bradykinin and other algesic agents - J. Comp. (springer.com)
  • The intracerebroventricular injection of bradykinin produces an increase in arterial blood pressure. (biomedsearch.com)
  • The increase in circulating bradykinin was associated with a decrease in the circulating level of bradykininogen, the precursor of bradykinin. (ahajournals.org)
  • In the present study, we report that cardiac bradykinin production is increased during anaphylaxis and that anaphylactic coronary vasoconstriction and ischemic arrhythmias, which are aggravated by bradykinin B 2 -receptor blockade, are in contrast alleviated by inhibitors of bradykinin breakdown. (ahajournals.org)
  • Using this approach, it was found that some bradykinin analogs are effective inhibitors of bradykinin. (wipo.int)
  • This tPA-triggered generation of bradykinin could participate in the deleterious effects of thrombolysis and is a potential target to improve neurological outcome in tPA-treated patients. (frontiersin.org)
  • The physiological role of C1-INH is to control the generation of bradykinin after activation of the contact system. (biomedcentral.com)
  • There are two kininogenases that convert kininogens into bradykinin: plasma kallikrein, also known as Fletcher factor, and glandular kallikrein, also known as tissue kallikrein. (hmdb.ca)
  • The B 1 receptor (also called bradykinin receptor B1 ) is expressed only as a result of tissue injury, and is presumed to play a role in chronic pain. (wikipedia.org)
  • However, little is known about the bradykinin receptor itself or its mechanisms of signal transduction, its function and its tissue distribution. (nih.gov)
  • Various bradykinin derivatives appear to exhibit different tissue specificity. (wipo.int)
  • In the rabbit hindleg lymph and tissue fluid were collected before and during close intraarterial infusions of histamine (2.5 and 10 micrograms/min) or bradykinin (0.4 microgram/min). (biomedsearch.com)
  • [12] Studies in our laboratory have demonstrated that sympathetic terminal synthesis and release of mediators, such as prostaglandins and purines, mediate bradykinin-induced synovial plasma extravasation and that sympathectomy or intraarticular indomethacin inhibits this process. (asahq.org)
  • The end result is a bradykinin storm, and according to the researchers, this appears to be an important factor in many of COVID-19's lethal effects, even more so than the cytokine storms associated with the disease. (mercola.com)
  • Evidence for this derives from studies of the interaction between bradykinin and its receptor, receptor-effector coupling systems and in vitro studies of the biological effects of bradykinin. (nih.gov)
  • It has not been possible to further evaluate the physiological effects of bradykinin during fetal and newborn life in the mouse or rat due to the limits imposed by size and immaturity. (physiology.org)
  • Even though potentially deadly side effects have been attributed to bradykinin, there is no experimental evidence. (ssc.ca)
  • We used combined patch-clamp-microfluorimetric recordings to examine the effects of bradykinin on [Ca2+]i transients and the Ca2+ current (ICa) in rat dorsal root ganglion neurons in vitro. (aspetjournals.org)
  • By using the same model, the present study was designed to investigate the effects of IL-1 beta and its interaction with TNF-alpha on the expression of bradykinin B-1 and B-2 receptors in mouse tracheal smooth muscle. (lu.se)
  • Additionally, albeit with a lower yield, des-Arg(9)-Met-Lys-bradykinin, an effective agonist of B1-subtype receptors, was released. (uni-muenchen.de)
  • Bradykinin acts through cell surface receptors to elicit a series of biological responses, many of which have been well characterized at the whole organ or body level. (nih.gov)
  • Microinjections in the medulla oblongata showed that the pressor responses were obtained when bradykinin was injected in the nucleus tractus solitarius or in the dorsal spinal trigeminal tract. (biomedsearch.com)
  • Bradykinin B1 and B2 receptors both have protective roles in renal ischemia/reperfusion injury. (nih.gov)
  • Thus, both the B1 and B2 bradykinin receptors play an important role in reducing DNA damage, apoptosis, morphological and functional kidney changes, and mortality during renal ischemia/reperfusion injury. (nih.gov)
  • In the kidney, B 2 receptors have been localized to cortical epithelium, medullary interstitium, and glomeruli and mesangial cells ( 13 ) and bradykinin, which activates B 2 receptors, is known to regulate renal hemodynamics as well as glomerular ultrafiltration and tubular function. (physiology.org)
  • SICUTERI F., FANCIULLACCI M., FRANCHI G. and DEL BIANCO P.L. (1965) - Serotonin-bradykinin potentiation on the pain receptors in man - Life Sc. (springer.com)