Aldosterone, inflammation, and preeclampsia.

We would like to suggest that aldosterone could play an important role in the genesis of this increased susceptibility of inflammatory process in preeclampsia. This contention comes from a number of our studies that provide rationale for this possibility. We have demonstrated that in preeclampsia, plasma aldosterone and plasma progesterone are as high as in uncomplicated pregnancy, whereas the rectal subtractive potential difference, which is an index of biological effect of aldosterone, is increased only in preeclampsia to a similar extent as in primary aldosteronism.2 These data are consistent also with the measurement of aldosterone receptors in mononuclear leukocytes, whose number was normal in uncomplicated pregnancy and downregulated in preeclampsia, which, again, matched the changes observed in primary aldosteronism.3 We therefore suggested that uncomplicated pregnancy is characterized by a reduced response to the action of aldosterone. In addition, we have recently demonstrated that the coincubation of human mononuclear leukocytes from healthy subjects with high concentrations of aldosterone induces the expression of 2 inflammation and oxidative stress-related proteins, plasminogen activator inhibitor-1 and p22phox, as shown by Western blot analysis. In the same study, we have also shown that these effects of aldosterone were blocked by the aldosterone receptor antagonist canrenone.4