kinin antagonists
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1995 ◽  
Vol 73 (7) ◽  
pp. 797-804 ◽  
Author(s):  
Klaus J. Wirth ◽  
Hoiger Heitsch ◽  
Bernward A. Schöikens

The availability of potent and stable bradykinin antagonists has had a tremendous impact on kinin research. This article reviews the current status of research on kinin antagonists, describes their chemical properties, and delineates recent advances that have occurred with the advent of the second generation of kinin antagonists. The data collected with these antagonists support the assumption that kinins are implicated in inflammation and tissue injury as endogenous agents. Their importance, however, is not limited to the role as mediators of tissue injury and inflammation, as kinin antagonists have enabled the identification of kinins as potential endogenous cardioprotective substances, also contributing to the effects of angiotensin converting enzyme inhibitors. Clinical studies are currently being performed in asthma, postoperative pain, anaphlyactoid reactions during low density lipoprotein apheresis, systemic inflammatory response syndrome, and suspected sepsis, head injury, and hantavirus infections to investigate the utility of kinin antagonists as therapeutic agents.Key words: bradykinin antagonists, chemistry, pharmacology, basic studies, clinical studies.


1992 ◽  
Vol 263 (5) ◽  
pp. R1136-R1140 ◽  
Author(s):  
F. J. Fenoy ◽  
R. J. Roman

The role of kinins in the natriuretic and papillary blood flow (PBF) responses to intravenous administration of 0.9% sodium chloride solution equal to 5% of body weight over 30 min was evaluated using a B1-kinin receptor antagonist (des-Arg9, [Leu8]bradykinin, 2.5 micrograms/min i.v.) and a B2-kinin receptor antagonist (D-Arg, [Hyp3,Thi5,8,D-Phe7]bradykinin, 2.5 micrograms/min i.v.). In control rats, PBF increased 43 +/- 5% after the volume expansion with saline. Administration of the B1-kinin receptor antagonist had no significant effect on basal PBF or the rise in PBF produced by volume expansion. In contrast, administration of the B2-kinin receptor antagonist decreased basal PBF by 18 +/- 3% and prevented the rise in PBF during volume expansion. Urine osmolality was lower in the rats treated with the B1-antagonist and higher in rats infused with the B2-kinin antagonist than in control animals after volume expansion (587 +/- 47 and 1,082 +/- 83 vs. 907 +/- 124 mosmol/kgH2O, respectively). The initial natriuretic response during the first 30 min after volume expansion was similar in rats given vehicle or the kinin antagonists. However, cumulative sodium excretion over the 2-h course of the experiment was significantly lower in the rats given the B2-receptor antagonist than in control rats (92 +/- 7 vs. 101 +/- 9% of the administered load). The B1-kinin receptor antagonist had no effect on cumulative sodium excretion; however, glomerular filtration rate was 30% lower in rats receiving the B1-antagonist than in control rats after volume expansion.(ABSTRACT TRUNCATED AT 250 WORDS)


The Lancet ◽  
1991 ◽  
Vol 338 (8773) ◽  
pp. 1011 ◽  
Author(s):  
JohnC. Cheronis ◽  
EricT. Whalley
Keyword(s):  

1990 ◽  
Vol 15 (Supplement) ◽  
pp. S69-S74 ◽  
Author(s):  
John M. Stewart ◽  
Raymond J. Vavrek
Keyword(s):  

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