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(Hypertension. 2007;49:e21.)
© 2007 American Heart Association, Inc.

Letters to the Editor

Modeling Preeclampsia: The True Model for the Uniquely Human Disease Preeclampsia Is the Human Female Not the Pregnant Rat

Blood Pressure Unit, Department of Cardiac and Vascular Sciences, St George’s University of London, London, United Kingdom

Isaac T. Manyonda

Department of Obstetrics and Gynaecology, St George’s University of London, London, United Kingdom

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

To the Editor:

Gadonski et al¹ describe a series of elegant experiments in which they used a rodent (rat) model to show that chronic reduction in uterine perfusion pressure was associated with an elevation of arterial pressure and that this elevation in AP was associated with a rise in serum levels of interleukin-6. They further showed that this rise in arterial pressure occurs after chronic elevation of interleukin-6 in pregnant but not in nonpregnant rats and is associated with increase in renal vascular resistance and reduction in renal plasma flow, as well as glomerular filtration rate. They conclude that interleukin-6 may play a role in mediating the hypertension and reduction in renal hemodynamics observed in the reduction in uterine perfusion pressure in pregnant rats. All of this is fine until the authors allude to the possibility that their observations could reflect the pathophysiology of that uniquely human disease of pregnancy, that is, preeclampsia (PE).

First, it is clear that no adequate laboratory model of PE exists. Stated another way, no animal model develops a condition during pregnancy that remotely resembles PE. This is in part because of the evolutionary diversity in placentation, and although the hemochorial placentation seen in the human also occurs in rodents, there are important differences between the 2 species. Specifically, rodents do not spontaneously develop PE. Occluding uterine arteries to create a reduction in uterine perfusion pressure could hardly be compared with the high resistance that is found in the fetoplacental circulation in PE. Moreover, studies . . . [Full Text of this Article]

This article has been cited by other articles:

				J. P. Granger Response to Modeling Preeclampsia: The True Model for the Uniquely Human Disease Preeclampsia Is the Human Female Not the Pregnant Rat Hypertension, April 1, 2007; 49(4): e22 - e22. [Full Text] [PDF]