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The Effect of Ischaemic-Reperfusion in Man - A Bradykinin Dependent Pathway

2014-08-27 03:19:49 | BioPortfolio

Summary

Heart attacks are usually caused by a blood clot blocking an artery supplying blood to the heart. Current treatments are designed to relieve this blockage as quickly as possible to minimize damage to the heart muscle. However in restoring the supply of blood local damage known as "ischaemia-reperfusion injury" may occur. 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. This will help the investigators to understand the mechanism by which ischaemia-reperfusion injury may occur and to devise new treatments for heart attacks.

Study Design

Allocation: Randomized, Control: Placebo Control, Intervention Model: Crossover Assignment, Masking: Double Blind (Investigator, Outcomes Assessor), Primary Purpose: Basic Science

Conditions

Ischaemic Heart Diseases

Intervention

Forearm vascular study, bradykinin receptor antagonist (HOE-140), Placebo (saline)

Location

University of Edinburgh, 49 Little France Crescent
Edinburgh
United Kingdom
EH16 4SB

Status

Recruiting

Source

University of Edinburgh

Results (where available)

View Results

Links

Published on BioPortfolio: 2014-08-27T03:19:49-0400

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Medical and Biotech [MESH] Definitions

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.

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 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 thiazole derivative and atypical ANTIPSYCHOTIC AGENT that functions as a DOPAMINE D2 RECEPTOR ANTAGONIST; SEROTONIN 5-HT2 RECEPTOR ANTAGONIST, serotonin 5-HT7 receptor antagonist, and antagonist of the adrenergic α2A and α2C receptors, as well as a partial SEROTONIN 5-HT1A RECEPTOR AGONIST. It is used in the treatment of SCHIZOPHRENIA and BIPOLAR DISORDER.

Compounds and drugs that inhibit ligand binding or cellular signaling by BRADYKININ B1 RECEPTORS.

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