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Kallikrein-kinin system activation and its interactions with other plasma haemostatic components in the coronary

M Czokało-Plichta1, E Skibinska, P Kosiorek

  • 1Department of General and Experimental Pathology, Medical Academy of Białystok, Białystok, Poland.

Roczniki Akademii Medycznej W Bialymstoku (1995)
|January 10, 2002
PubMed

Insights

Exercise activates fibrinolysis and prekallikrein in coronary artery disease (CAD) patients. Kininogen and kallikrein may regulate endothelial hemostasis, with bradykinin potentially inducing tissue plasminogen activator (t-PA) secretion.

Area of Science:

  • Cardiovascular Medicine
  • Hemostasis and Thrombosis
  • Biochemistry

Background:

  • Coronary artery disease (CAD) involves complex hemostatic and fibrinolytic system alterations.
  • Understanding the dynamic changes in these systems during physiological stress like exercise is crucial for patient management.

Purpose of the Study:

  • To investigate the impact of exercise on plasma kininogens, prekallikrein, fibrinogen, protease inhibitors, and related enzymatic activities in CAD patients.
  • To explore the potential roles of the kinin-kallikrein system and endothelial cells in regulating fibrinolysis during exercise in CAD.

Main Methods:

  • Blood samples were collected from 44 stable CAD patients and 54 myocardial infarction patients (treated/untreated with ACE inhibitors) before and after an exercise test.
  • Assessed concentrations of kininogens, prekallikrein, fibrinogen, protease inhibitors, and activities of kininase, fibrinolytic, and antipapain.
  • Patients were subgrouped based on treatment with angiotensin I-converting enzyme inhibitor (ACE-I) enalapril.

Main Results:

  • Exercise induced activation of the fibrinolytic system and prekallikrein in CAD patients.
  • No significant kininogen consumption was observed, but kininase activity decreased post-exercise.
  • Findings suggest endothelial cells contribute to plasminogen activation, potentially mediated by kallikrein and bradykinin-induced t-PA secretion.

Conclusions:

  • The kinin-kallikrein system, possibly via released kinins, may play a role in regulating endothelial hemostatic functions in CAD.
  • Exercise stimulates fibrinolysis and prekallikrein activation, with bradykinin potentially enhancing tissue plasminogen activator (t-PA) release, influenced by increased blood flow.

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