It can be recovered from ovarian follicular fluid. Ovarian prorenin might be involved in the pathogenicity of ovarian hyperstimulation syndrome as, in this circumstance, very high values of total renin, renin activity and aldosterone, unsuppressed by fluid overload, have been reported. The level of prorenin in follicular fluid could have a prognostic value as a marker for the chance of survival of transplanted eggs. At term pregnancy, inactive renin has been localized by the immunofluorescent technique in trophoblasts of the human chorion laeve. This terminal active peptide of the renin-converting enzyme cascade increases in consequence of the rise of renin activity or of active renin.
Urinary aldosterone increases steadily up to the last week of gestation.
This increase partly results from increased renin activity and partly counteracts the opposing effect of increased progesterone which exerts an antialdosterone effect. From these findings, one may assume that no changes of angiotensin II binding sites occur on the zona glomerulosa cells of the adrenal cortex, contrary to what has been observed in platelets and inferred to occur in vascular smooth muscle cells. Atrial natriuretic hormone Plasma ANP concentration increases significantly during the third trimester of uncomplicated pregnancy with a further rise 72 h postpartum. It might also be involved in steroidogenesis. Increased levels have been found in patients with preeclampsia and could play a role in its pathogeny by aggravating fetal hypoxia through its vasoconstrictor effect on the placental vascular bed.