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Published on: October 26, 2020
Portal hypertensive response to kinin
Maria Kouyoumdjian1, Marcia R Nagaoka, Mauricio R Loureiro-Silva
1Laboratório de Hepatologia Experimental, UNIFESP, São Paulo, SP, Brasil.
Anais Da Academia Brasileira De Ciencias
|September 2, 2009
Summary
Bradykinin increases resistance in liver blood vessels via B2 receptors, a mechanism unchanged by liver disease. Angiotensin converting enzyme degrades bradykinin after its hypertensive effect.
Area of Science:
- Hepatology
- Vascular Biology
- Pharmacology
Background:
- Portal hypertension, a common complication of chronic liver diseases like cirrhosis, stems from increased intrahepatic vascular resistance.
- This resistance is linked to cellular architectural changes and stellate cell contraction.
- The kallikrein-kinin system and its role in disease development are areas of interest.
Purpose of the Study:
- To investigate the role of bradykinin in normal and experimental models of hepatic injury.
- To elucidate the mechanisms underlying bradykinin-induced changes in intrahepatic vascular resistance.
Main Methods:
- Utilized isolated rat liver perfusion models (mono and bivascular).
- Employed isolated liver cells for experimental analysis.
- Reviewed historical aspects of the kallikrein-kinin system.
Main Results:
- Bradykinin-induced increase in intrahepatic vascular resistance is mediated by B2 receptors, involving sinusoidal endothelial and stellate cells, and persists in inflammation, fibrosis, and cirrhosis.
- The hepatic arterial hypertensive response to bradykinin is calcium-independent and eicosanoid-mediated.
- Bradykinin lacks a vasodilating effect on pre-constricted perfused rat livers.
- Angiotensin converting enzyme degrades bradykinin following its hypertensive effect.
Conclusions:
- The hypertensive response to bradykinin is consistently mediated by the B2 receptor in both normal and pathological liver conditions.
- The B1 receptor shows increased expression in regenerating and cirrhotic livers, warranting further investigation into its role.
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