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DOI: 10.1055/s-2003-43503
Umbilical Plasma Kininase I Activity in Fetal Hypoxia
Publication History
Received 25 February 2003
Accepted after revision 12 June 2003
Publication Date:
07 November 2003 (online)
Abstract
To shed light on the role of bradykinin in preeclampsia in addition to acute hypoxia, we measured the activity of kininase I, the enzyme responsible for its degradation, in umbilical plasma. Kininase I activity in umbilical arteries was compared with that in the umbilical veins. The relationship between kininase I and pH values was also evaluated in women with and without preeclampsia. Also, enzyme activity in supernatants of fetal hepatic cells (NFL/T) cultured under hypoxic or normoxic conditions were determined. Kininase I activity levels in fetal umbilical arteries and veins (n = 33) were similar (r = 0.77). Hypoxia caused suppression of kininase I activity in the supernatant cultures of NFL/T after one hour. However, after 8 and 24 hours, kininase I activity was significantly greater than under normoxic conditions (p < 0.05). Kininase I activity of fetal umbilical vein significantly decreased in the presence of acidemia in the uncomplicated group (n = 75, r = 0.42), whereas the activity negatively correlated with umbilical arterial pH in the preeclamptic group (n = 10, r = - 0.65). Kininase I activity levels in cases complicated with preeclampsia were significantly higher than without preeclampsia (49.2 ± 9.1 vs. 66.2 ± 11.3 nmol/ml/min). The present study indicates that kininase I acts as a regulatory factor in bradykinin degradation.
Key words
Kininase I - Bradykinin - Umbilical blood - Preeclampsia - Fetal hepatic cell
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A. Itakura, M. D.
Maternity and Perinatal Care Center · Nagoya University Hospital
65 Tsurumai-cho · Showa-ku · Nagoya 466-8550 · Japan
Fax: + 81(52)744-2268
Email: aita@med.nagoya-u.ac.jp