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(Hypertension. 2005;45:e10.)
© 2005 American Heart Association, Inc.

Letter to the Editor

Aldosterone, Inflammation, and Preeclampsia

Department of Medical and Surgical Sciences and Department of Clinical and Experimental Medicine, University of Padua, Italy.

An extract of the first 250 words of the full text is provided, because this article has no abstract.

To the Editor:

We read with great interest the recent article published by Freeman et al in the November issue of Hypertension,¹ which focuses on a possible systemic inflammatory response in patients with preeclampsia. The authors suggest that the susceptibility to inflammation might be a common underlying risk factor for preeclampsia and conclude that the mechanism for this inflammatory susceptibility is unknown and could be attributable to a generalized upregulation of several inflammatory processes.

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 p22^phox, as shown . . . [Full Text of this Article]

This article has been cited by other articles:

				B. D. LaMarca, J. Gilbert, and J. P. Granger Recent Progress Toward the Understanding of the Pathophysiology of Hypertension During Preeclampsia Hypertension, April 1, 2008; 51(4): 982 - 988. [Full Text] [PDF]