Dr Maria Kouyoumdjian, Rua Botucatu 862 (Edifício José Leal Prado), 04023-900 São Paulo, Brazil. Email: [email protected]Search for more papers by this author

Leda Teixeira Carvalho,

Leda Teixeira Carvalho

Departments of Biochemistry and

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Écio Alves Nascimento,

Écio Alves Nascimento

Department of Biochemistry, State University of Maringá, Paraná, Brazil

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Felipe Oliveira Teixeira,

Felipe Oliveira Teixeira

Experimental Hepatology Laboratory, UNIFESP, São Paulo and

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Márcia Regina Nagaoka,

Márcia Regina Nagaoka

Departments of Biochemistry and

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Durval Rosa Borges,

Durval Rosa Borges

Medicine, Federal University of São Paulo,

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Maria Kouyoumdjian,

Corresponding Author

Maria Kouyoumdjian

Departments of Biochemistry and

Dr Maria Kouyoumdjian, Rua Botucatu 862 (Edifício José Leal Prado), 04023-900 São Paulo, Brazil. Email: [email protected]Search for more papers by this author

First published: 15 August 2007

https://doi.org/10.1111/j.1440-1746.2007.05074.x

Citations: 6

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Abstract

Background and Aim: Angiotensin I (AI) and angiotensin II (AII) induce a portal hypertensive response (PHR) and the liver is able to convert AI into AII to trough the action of the angiotensin-converting enzyme (ACE). Our purpose was to characterize angiotensin I liver conversion.

Methods: AI, AII or angiotensin (1–7) were used in monovascular or bivascular perfusions.

Results: The maximum gain in portal pressure induced by AII took place significantly earlier (P = 0.031) than that occurring after an equimolar AI infusion. The AI-induced PHR was abolished both by captopril or losartan, whereas the AII-induced PHR was not affected by captopril, but was abolished by losartan. Angiotensin (1–7) has no hemodynamic effect in the perfused liver. After partial hepatectomy, the AII–PHR pattern changes from a rapid return to baseline values to a pattern where there was no return to baseline values (3–7 days ex-surgery). In the bivascular perfusion system when AII was infused in the arterial branch in the retrograde mode of perfusion (peptide available only to the periportal zone), the PHR was at least 50% of that obtained when the prograde mode was used (peptide available to the periportal and perivenous zones).

Conclusion: AI does not induce PHR; this effect is a result of its mandatory conversion into AII by the ACE and the sequential action of AII on the AII receptor type 1 located in the hepatic periportal zone. AII induced PHR pattern changes during liver regeneration.

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Volume22, Issue9

September 2007

Pages 1543-1548

Hepatic conversion of angiotensin I and the portal hypertensive response to angiotensin II in normal and regenerating liver

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Hepatic conversion of angiotensin I and the portal hypertensive response to angiotensin II in normal and regenerating liver

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