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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
PubMed

Insights

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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