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2 edition of interrelationship between bradykinin and cyclo-oxygenase products in the rat small intestine. found in the catalog.

interrelationship between bradykinin and cyclo-oxygenase products in the rat small intestine.

Roger Walker

interrelationship between bradykinin and cyclo-oxygenase products in the rat small intestine.

by Roger Walker

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Published by University of Aston in Birmingham. Department of Pharmacy in Birmingham .
Written in English


Edition Notes

SeriesPh.D. thesis
ID Numbers
Open LibraryOL21001215M

Bradykinin and related kinins are a family of small peptides which act as mediators of pain and exert a variety of biological effects on the endothelium and peripheral circulation through their action on two G-protein-coupled bradykinin receptor subtypes, the B 1 receptor and the B 2 receptor. Bradykinin is an important pro-inflammatory molecule that causes vasodilation. Cyclooxygenase (COX) products play an important role in modulating sepsis and subsequent endothelial injury. We hypothesized that COX inhibitors may attenuate endothelial dysfunction during sepsis, as measured by receptor-mediated bradykinin (BK)-induced vasoconstriction and/or receptor-independent hypoxic pulmonary vasoconstriction (HPV).

Interstitial fluid bradykinin levels are reported to be in the 10– nM range in both cortex and medulla regions of the rat kidney. These concentrations are considerably higher than those present in the bloodstream [ 26 ] and more than sufficient to effectively stimulate B2R [ 27, 28 ]. Key points. Bradykinin may play a role in the autodigestive disease acute pancreatitis, but little is known about its pancreatic actions. In this study, we have investigated bradykinin‐elicited Ca 2+ signal generation in normal mouse pancreatic lobules.; We found complete separation of Ca 2+ signalling between pancreatic acinar (PACs) and stellate cells (PSCs).

Bradykinin is a potent vasodilator that acts through endothelial B2 kinin receptors to stimulate the release of nitric oxide and endothelium-derived hyperpolarizing factor. Bradykinin deficiency states may play a role in some forms of hypertension, and a relative deficiency in bradykinin may be a contributing factor to worsening heart failure. Abstract. In this report, we show that desensitization regulates ligand-independent, spontaneous activity of the human B2 bradykinin (BK) receptor, and the level of spontaneous receptor activity determines the action of the BK antagonists and partial receptor agonists NPC and HOE as .


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Interrelationship between bradykinin and cyclo-oxygenase products in the rat small intestine by Roger Walker Download PDF EPUB FB2

The interrelationship between bradykinin and cyclo-oxygenase products in the rat small intestine Author: Walker, Roger ISNI: Awarding Body: University of Aston in Birmingham Current Institution: Aston University Date of Award: Author: Roger Walker.

The interrelationship between bradykinin and cyclo-oxygenase products in the rat small intestine By Roger Walker OAI identifier: oai:or: Roger Walker.

Overview of coagulation, contact activation and fibrinolysis. The coagulation cascade is initiated by either tissue factor (TF) or FXIIa. Positive feedback by thrombin (FIIa) accelerates coagulation. The end-product of coagulation is fibrin, cross-linked by factor is degraded by this process, D-dimer, an important clinical biomarker for thrombosis, is by: A novel herbal preparation desensitizes mesenteric afferents to bradykinin in the rat small intestine Article in Neurogastroenterology and Motility 21(4) December with 33 Reads.

Bradykinin is a naturally occurring nonapeptide which plays a pivotal role in the production of pain and inflammation. Most of the physiological actions of bradykinin have been ascribed to activation of the B 2 receptor, linked to intracellular events that involve the generation of diacylglycerol and inositol triphosphates (see Levine et al.

).The site of B 1 receptors remains to be Cited by: Responses to bradykinin and LPS (1 and 5 μg) were inhibited by the cyclo‐oxygenase inhibitor, indomethacin and by the β‐adrenoceptor antagonist, atenolol.

The effects of indomethacin and atenolol were additive: their combination abolished responses to bradykinin and LPS (1 μg) and markedly attenuated the response to LPS (5 μg). The selective bradykinin B1 receptor agonist des-Arg9-bradykinin (10(-6) M) caused a small relaxation (+/%, n=6), which could be antagonized completely by the selective bradykinin B1.

In C9 rat liver cells bradykinin and kallidin increased (∼ 2‐fold) the intracellular concentration of calcium, but the B1 agonist, des‐Arg9‐bradykinin did not. The effect of bradykinin was inhibited by the B2 antagonists, Hoe and N‐α‐adamantaneacetyl‐D‐Arg‐[Hyp3, Thi, D‐Phe7]‐bradykinin, but not by.

NSAIDs inhibit cyclo‐oxygenase‐2 at the site of inflammation, to produce their therapeutic benefits, as well as cyclo‐oxygenase‐1 in the gastric mucosa, which produces gastric damage.

Most recently selective inhibitors of cyclo‐oxygenase‐2 have been developed and introduced to man for the treatment of. A pathogenetic role for bradykinin in osteoarthritis has been hypothesized (Meini and Maggi, ), and there is evidence that, when injected in the rat knee joint, BK causes a progressive.

Gen. Pharmac. Vol. 19, No. 2, pp./88 $+ Printed in Great Britain. All rights reserved Copyright Pergamon Journals Ltd MINIREVIEW. The bradykinin antagonist CP can limit the progression of post‐ischemic pancreatitis.

Immunopharmacol – Hu H‐Z, Gao N, Liu S, Ren J, Wang X, Xia Y & Wood JD (). Action of bradykinin in the submucosal plexus of guinea pig small intestine.

J Pharmacol Exp Ther– Israili ZH & Hall WD (). Bradykinin levels are elevated locally at the site of swelling in HAE [25,4].

A unique family in which a mutation of C1 INH renders it inactive on activated C1 but normally active as an inhibitor of the enzymes of the bradykinin-forming cascade (ie, Factor XIIa, Factor XIIf, and kallikrein) has no episodes of angioedema in any family members.

Sheep anti‐rat IL‐1β, sheep anti‐human IL‐8 and sheep anti‐rat IL‐6 antisera were from the National Institute for Biological Standards and Control (NIBSC, Hertfordshire, England) and were generous gifts from Dr Stephen Poole.

Statistical analysis. All results are. Responses to bradykinin and LPS (1 and 5 μg) were inhibited by the cyclo‐oxygenase inhibitor, indomethacin and by the β‐adrenoceptor antagonist, atenolol.

The effects of indomethacin and atenolol were additive: their combination abolished responses to bradykinin and LPS (1 μg) and markedly attenuated the response to LPS (5 μg).

Although bradykinin undergoes extensive inactivation by endothelial peptidases, including ACE, on passage through the lungs, commonly a small fraction of the peptide survives []. Bradykinin contains three pro- line residues, and the cis-trans ratio of each of the imide bonds has been estimated to be up to 10% at equilibrium [33, 34].

with the stomach or intestine. Bradykinin by a small bradykinin dose together with peptidase inhibitors. there appears to be an inter-relationship between cytokines and kinins in the.

bradykinin can be directly released from HK by other en-zymes than PK; this was recently demonstrated for Mannose Binding Serine Protease 1 [58]. The relevance of these FXII-independent pathways of bradykinin generation needs to be established.

It is imaginable that during endothelial cell activation or damage, small amounts of PPK are. Bradykinin is a potent endothelium-dependent vasodilator and acts via the bradykinin B2 receptor (encoded by BDKRB2; location: 14qq).

The absence (− 9), rather than the presence (+ 9), of a 9-bp repeat sequence in exon 1 has previously been shown to be associated with increased gene transcription and higher BDKRB2 mRNA expression. The role of cPLA 2 in brain trauma remains unknown. Therefore, we examined samples from TBI patients and rat brain cortices after CCI to examine the impact and changes of cPLA 2 levels following brain examined protein expression and found that levels of cPLA 2 and bradykinin B2 receptor (Fig.

1A). In both the. Lack of Bradykinin Receptors and Diabetic Nephropathy. Urinary albumin excretion, already approximately × normal in the Akita diabetic mice and approximately × and approximately × normal in the B2R-null and BRKO mice, is increased to approximately × and approximately × normal in the B2R-null and BRKO-Akita mice and there is a strong positive interaction between .Interestingly, the mouse B2 bradykinin receptor has a fold higher affinity than the human B2 bradykinin receptor for the peptide antagonists D-Arg0[Hyp3,Thi5,8,D-Phe7]bradykinin and D-Arg0.Ensembl ENSG ENSMUSG UniProt P P RefSeq (mRNA) NM_ NM_ RefSeq (protein) NP_ NP_ Location (UCSC) Chr – Mb Chr – Mb PubMed search Wikidata View/Edit Human View/Edit Mouse Bradykinin receptor B 2 is a G-protein coupled receptor for bradykinin, encoded by the BDKRB2 .