Activation of the blood kallikrein-kinin system during disseminated intravascular clotting in rats. role of the pulmonary component and attempted correction with aspirin

1984 ◽  
Vol 98 (3) ◽  
pp. 1176-1179
Author(s):  
G. N. Meshcheryakov ◽  
O. A. Gomazkov
Keyword(s):  
Kinin System ◽  
Kallikrein Kinin System ◽  
Disseminated Intravascular Clotting

scholarly journals Kinins and Kinin Receptors in Cardiovascular and Renal Diseases

2021 ◽  
Vol 14 (3) ◽  
pp. 240
Author(s):  
Jean-Pierre Girolami ◽  
Nadine Bouby ◽  
Christine Richer-Giudicelli ◽  
Francois Alhenc-Gelas
Keyword(s):  
Experimental Studies ◽  
Physiological Role ◽  
Renal Diseases ◽  
Kinin System ◽  
Genetic Studies ◽  
Pharmacological Manipulation ◽  
Kininase Ii ◽  
Kinin Receptors ◽  
Kallikrein Kinin System

This review addresses the physiological role of the kallikrein–kinin system in arteries, heart and kidney and the consequences of kallikrein and kinin actions in diseases affecting these organs, especially ischemic and diabetic diseases. Emphasis is put on pharmacological and genetic studies targeting kallikrein; ACE/kininase II; and the two kinin receptors, B1 (B1R) and B2 (B2R), distinguished through the work of Domenico Regoli and his collaborators. Potential therapeutic interest and limitations of the pharmacological manipulation of B1R or B2R activity in cardiovascular and renal diseases are discussed. This discussion addresses either the activation or inhibition of these receptors, based on recent clinical and experimental studies.

Role of kallikrein-kinin system in pathogenesis of bacterial cell wall-induced inflammation

1991 ◽  
Vol 260 (2) ◽  
pp. G213-G219 ◽  
Author(s):  
R. A. DeLa Cadena ◽  
K. J. Laskin ◽  
R. A. Pixley ◽  
R. B. Sartor ◽  
J. H. Schwab ◽  
...  
Keyword(s):  
Cell Wall ◽  
Acute Phase ◽  
Bacterial Cell ◽  
Chronic Phase ◽  
Bacterial Cell Wall ◽  
Kinin System ◽  
Kallikrein Kinin System ◽  
Bacterial Products

The plasma kallikrein-kinin system is activated in Gram-negative sepsis and typhoid fever, two diseases in which bacterial products have been shown to initiate inflammation. Because a single intraperitoneal injection of bacterial cell wall peptidoglycan-polysaccharide polymers from group A steptococci (PG-APS) into a Lewis rat produces a syndrome of relapsing polyarthritis and anemia, we investigated changes in the role of the kallikrein-kinin system in this model of inflammation. Coagulation studies after injection of PG-APS revealed an immediate and persistent decrease in prekallikrein levels. High-molecular-weight kininogen levels decreased significantly during the acute phase and correlated with the severity of arthritis. Factor XI levels were decreased only during the acute phase. Antithrombin III levels remained unchanged, indicating that neither decreased hepatic synthesis nor disseminated intravascular coagulation caused the decreased plasma contact factors. Plasma T-kininogen (an acute phase protein) was significantly elevated during the chronic phase. PG-APS failed to activate the contact system in vitro. Thus the kallikrein-kinin system plays an important role in this experimental model of inflammation, suggesting that activation of this system may play a role in the pathogenesis of inflammatory bowel disease and rheumatoid arthritis in which bacterial products might be etiologically important.

The dual role of the contact system in bacterial infectious disease

2007 ◽  
Vol 98 (09) ◽  
pp. 497-502 ◽  
Author(s):  
Inga-Maria Frick ◽  
Lars Björck ◽  
Heiko Herwald
Keyword(s):  
Vascular Endothelium ◽  
Blood Cells ◽  
State Of The Art ◽  
Contact System ◽  
Intrinsic Pathway ◽  
Kinin System ◽  
Inflammatory Reactions ◽  
Bacterial Infectious Disease ◽  
Kallikrein Kinin System

SummaryHemostasis is a sensitive and tightly regulated process, involving the vascular endothelium and blood cells as well as factors of the coagulation and fibrinolytic cascades. Over the last four decades evidence has accumulated that during infection, inflammatory mediators from the microbe and/or host are capable to modulate the equilibrium between the procoagulant and anticoagulant status of the host. Dependent on the mode of activation, these changes can cause either local or systemic inflammatory reactions that may be beneficial or deleterious to the human host. The present review aims to present the state of the art with respect to the role of the contact system (also known as the intrinsic pathway of coagulation or the kallikrein/kinin system) in innate immunity and systemic inflammatory reactions.

scholarly journals Antihypertensive effect of MK-421 in rats. Role of the renal kallikrein-kinin system.

Hypertension ◽  
1984 ◽  
Vol 6 (2_pt_1) ◽  
pp. 229-235 ◽  
Author(s):  
M Yasujima ◽  
K Abe ◽  
M Tanno ◽  
Y Kasai ◽  
J Tajima ◽  
...  
Keyword(s):  
Antihypertensive Effect ◽  
Kinin System ◽  
Renal Kallikrein ◽  
Kallikrein Kinin System

scholarly journals A Role of Inflammation and Immunity in Essential Hypertension—Modeled and Analyzed Using Petri Nets

2020 ◽  
Vol 21 (9) ◽  
pp. 3348
Author(s):  
Dorota Formanowicz ◽  
Agnieszka Rybarczyk ◽  
Marcin Radom ◽  
Piotr Formanowicz
Keyword(s):  
Essential Hypertension ◽  
Adaptive Immune System ◽  
Low Grade ◽  
Kinin System ◽  
Reactive Protein ◽  
Adaptive Immune ◽  
Key Enzyme ◽  
Kallikrein Kinin System ◽  
Low Grade Inflammation

Recent studies have shown that the innate and adaptive immune system, together with low-grade inflammation, may play an important role in essential hypertension. In this work, to verify the importance of selected factors for the development of essential hypertension, we created a Petri net-based model and analyzed it. The analysis was based mainly on t-invariants, knockouts of selected fragments of the net and its simulations. The blockade of the renin-angiotensin (RAA) system revealed that the most significant effect on the emergence of essential hypertension has RAA activation. This blockade affects: (1) the formation of angiotensin II, (2) inflammatory process (by influencing C-reactive protein (CRP)), (3) the initiation of blood coagulation, (4) bradykinin generation via the kallikrein-kinin system, (5) activation of lymphocytes in hypertension, (6) the participation of TNF alpha in the activation of the acute phase response, and (7) activation of NADPH oxidase—a key enzyme of oxidative stress. On the other hand, we found that the blockade of the activation of the RAA system may not eliminate hypertension that can occur due to disturbances associated with the osmotically independent binding of Na in the interstitium. Moreover, we revealed that inflammation alone is not enough to trigger primary hypertension, but it can coexist with it. We believe that our research may contribute to a better understanding of the pathology of hypertension. It can help identify potential subprocesses, which blocking will allow better control of essential hypertension.

Role of the kallikrein-kinin system of the kidneys in sodium and water transport and its modification by indomethacin

1977 ◽  
Vol 83 (4) ◽  
pp. 456-458 ◽  
Author(s):  
A. A. Nekrasova ◽  
E. A. Zharova ◽  
R. I. Sokolova
Keyword(s):  
Water Transport ◽  
Kinin System ◽  
Kallikrein Kinin System

scholarly journals The role of the renal kallikrein-kinin system in sodium metabolism in normal and low renin essential hypertension.

1983 ◽  
Vol 47 (10) ◽  
pp. 1210-1215 ◽  
Author(s):  
KAZUAKI SHIMAMOTO ◽  
TAKASHI NAKAO ◽  
NOBUYUKI URA ◽  
SHIGEMICHI TANAKA ◽  
TOSHIAKI ANDO ◽  
...  
Keyword(s):  
Essential Hypertension ◽  
Kinin System ◽  
Renal Kallikrein ◽  
Sodium Metabolism ◽  
Kallikrein Kinin System

The role of the kallikrein-kinin system in joint inflammatory disease

1991 ◽  
Vol 23 (2) ◽  
pp. 105-112 ◽  
Author(s):  
J.N. Sharma
Keyword(s):  
Inflammatory Disease ◽  
Kinin System ◽  
Kallikrein Kinin System
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