Summary
The role of microsomal placental leucine aminopeptidase (microsomal P-LAP) in the
decreased pressor responsiveness to angiotensin II (A-II) in pregnancy was studied.
Appreciable amounts of microsomal P-LAP activity were found in rat placenta. The similar
dose to the endogenous activity, of human microsomal P-LAP exogenously administered
to rats, resulted in significant decrease in the response to A-II. Bestatin, an inhibitor
of the microsomal leucine aminopeptidase administered to pregnant rats, enhanced the
A-II response. Therefore our present study suggests such refractoriness in response
to A-II in pregnancy is due to increased inactivation by the microsomal P-LAP. It
was also suggested that prostaglandins were not involved in such refractoriness by
the experiments with indomethacin.
Key words
Angiotensin II - Microsomal P-LAP - Blunted pressor response to A-II - Placental angiotensinases
- Hypertension
