Download PDF
Exp Clin Endocrinol Diabetes 1987; 90(5): 206-212
DOI: 10.1055/s-0029-1210691
Original

© J. A. Barth Verlag in Georg Thieme Verlag KG Stuttgart · New York

Effect of Microsomal Leucine Aminopeptidase from Human Placenta (microsomal P-LAP) on Pressor Response to Infused Angiotensin II (A-II) in Rat

S. Mizutani, H. Taira, O. Kurauchi, Y. Ito, H. Imaizumi, M. Furuhashi, O. Narita, Y. Tomoda
  • Department of Obstetrics and Gynecology (Director: Prof. Yutaka Tomoda), Nagoya University School of Medicine, Nagoya/Japan
Further Information

Publication History

1986

Publication Date:
16 July 2009 (online)

Also available at
  PDF Download  Permissions and Reprints

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