Plasma Kallikrein Inhibitors in Cardiovascular Disease

2016 ◽  
Vol 24 (3) ◽  
pp. 99-109 ◽  
Author(s):  
Dhaval Kolte ◽  
Zia Shariat-Madar
2001 ◽  
Vol 49 (11) ◽  
pp. 1457-1463 ◽  
Author(s):  
Yuko TSUDA ◽  
Mayako TADA ◽  
Keiko WANAKA ◽  
Utako OKAMOTO ◽  
Akiko HIJIKATA-OKUNOMIYA ◽  
...  

1973 ◽  
Vol 45 (4) ◽  
pp. 429-438
Author(s):  
M. Malofiejew

1. The plasma of non-pregnant women contains practically no kinins and only traces of kallikrein. Treatment of the plasma with kaolin produces additional amounts of kallikrein from prekallikrein and of kinin from kininogen. 2. During the second stage of labour, plasma kallikrein is increased and the amount of kallikrein inhibitors is decreased. The plasma kinin-forming activity is only slightly increased due, apparently, to a fall in plasma kininogen. 3. Plasma kallikrein causes a rise in the contractile tonus of the isolated rat and human myometrium.


1977 ◽  
Author(s):  
M. J. Gallimore ◽  
A. O. Aasen ◽  
E. Amundsen

Plasma protease activity is known to be increased during endotoxin shock and recent studies have indicated that the plasma kallikrein-kinin system becomes activated by circulating endotoxin. Plasma levels of pre-kallikrein kallikrein and kallikrein inhibitors were therefore determined in samples from dogs infused with E. coli endotoxin, using assays with a chromogenic substrate for plasma kallikrein(Chromozyme -PK, Pentapharm, Basle, Switzerland). “Fast-reacting” and “time-dependent” inhibitors of kallikrein were studied using purified human plasma kallikrein. Considerably reduced levels of plasma pre-kallikreiri and increased levels of kallikrein were detected in the late phase of shock and significant reductions in “fast-reacting” and “time-dependent” inhibition of kallikrein was observed. These results show that during endotoxin shock plasma pre-kallikrein becomes activated to kallikrein and indicate that kallikrein inhibitors play an important mediatory role in the pathophysiology of endotoxin shock.


1993 ◽  
Vol 41 (6) ◽  
pp. 1079-1090 ◽  
Author(s):  
Naoki TENO ◽  
Keiko WANAKA ◽  
Yoshio OKADA ◽  
Hiroaki TAGUCHI ◽  
Utako OKAMOTO ◽  
...  

2016 ◽  
Vol 8 (2) ◽  
pp. 185-190 ◽  
Author(s):  
Zhe Li ◽  
James Partridge ◽  
Abel Silva-Garcia ◽  
Peter Rademacher ◽  
Andreas Betz ◽  
...  

2020 ◽  
Author(s):  
Ada Admin ◽  
Miran A Jaffa ◽  
Ionut Bebu ◽  
Deirdre Luttrell ◽  
Barbara H Braffett ◽  
...  

We determined the relationship between plasma kallikrein and cardiovascular disease (CVD) outcomes as well as major adverse cardiovascular events (MACE) in the DCCT/EDIC-cohort of type 1 diabetes (T1D). Plasma kallikrein levels were measured longitudinally in 693 subjects at DCCT baseline (1983-1989), mid-point of DCCT (1988-1991), end of DCCT (1993), and EDIC years 4-6 (1997-1999), 8-10 (2001-2003), and 11-13 (2004-2006). Cox proportional hazards regression models assessed the association between plasma kallikrein levels and the risk of CVD. In unadjusted models, higher plasma kallikrein levels were associated with higher risk of any CVD during DCCT/EDIC (HR=1.16 per 20 nM higher levels of plasma kallikrein; p=0.0177) as well as over the EDIC-only period (HR=1.22; p=0.0024). The association between plasma kallikrein levels and the risk of any CVD remained significant during the EDIC follow-up after adjustment for age and mean HbA1c (HR=1.20; p=0.0082) and in the fully adjusted model for other CVD risk factors (HR=1.17; p=0.0330). For MACE, higher plasma kallikrein levels were associated with higher risk in unadjusted (HR=1.25; p=0.0145), minimally adjusted (HR=1.23; p=0.0417, and fully adjusted (HR=1.27; p=0.0328) models during EDIC-only. These novel findings indicate that plasma kallikrein level associates with the risk of any CVD and MACE in T1D individuals.


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