Larmie, E.T. and Singh, Harbindar Jeet and Shukri, Mohd
(2004)
Kallikrein-kinin system in human
fetoplacental tissues in
pregnancy -induced
hypertension.
Kallikrein-kinin system in human fetoplacental tissues in pregnancy -induced hypertension.
(Submitted)
Abstract
The pathogenesis·~ of pregnancy-induced ···hypertension·· (Pil-l) remains an
enigma. However, it is currently postulated that placental hypoperfusion due
to an imbalance of vasoconstrictor and vasodilator substances in the placenta
may contribute to the pathogenesis of PIH. Hence, the objectives of this study
are: (1) to determine the kininogen {using enzyme immunoassay) and tissue
kallikrein levels (using a synthetic chromogenic substrate, S-2266), the
substrate and enzyme, respectively, that are responsible for the generation of
kinin (a vasodilator); (2) to determine the molecular weight of tissue kallikrein
(by Western blot analysis); and (3) to determine the gross effect of
fetoplacental tissue extracts on the contraction of rabbit jejunum smooth
muscle using various fetoplacental tissues from 12 normotensive pregnant
women and 12 women with PIH. No significant differences were found for
active, total and inactive tissue kallikrein levels in tissues from both groups.
However, kininogen levels and kininogen/total tissue kallikrein ratios were
significantly lower in chorion laeve, placental plate chorion, fetal placenta and
maternal placenta from women with PIH. The molecular weight of tissue
kallikrein was about 52 kDa for both groups. These findings might indicate a
lower level of kinin generation in fetoplacental tissues of women with PIH
confirming the reported preponderance of vasoconstrictor activity. The higher
increase in smooth muscle tone produced by application of the fetoplacental
tissue extracts from women with PIH also further supports this postulate.
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