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(Hypertension. 2007;49:e22.)
© 2007 American Heart Association, Inc.

Letters to the Editor

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

University of Mississippi Medical Center, Jackson, Miss

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

We recently reported in Hypertension¹ that the elevation in arterial pressure in pregnant rats with placental ischemia was associated with significant increases in serum interleukin (IL)-6. Moreover, we found that chronic elevation in serum levels of IL-6, comparable to levels observed in our placental ischemic pregnant rat model, resulted in significant increases in arterial pressure and decreases in renal hemodynamics in pregnant rats. These results led us to conclude that IL-6 may play a role in mediating the hypertension and reduction in renal hemodynamics observed with placental ischemia in pregnant rats.¹

Nama et al² expressed concerns and indicated that "there is no adequate laboratory model of preeclampsia" and that no animal model "develops a condition during pregnancy that remotely resembles preeclampsia." They also suggested that, "any significant progress in the field of preeclampsia research can only realistically come from studies of the human model."

Although we agree that rats may not spontaneously develop preeclampsia, we believe that our rat model provides an excellent opportunity to study the relationship between placental ischemia and hypertension. Although placental ischemia has been proposed to lead to widespread endothelial dysfunction, vasoconstriction, and hypertension in the maternal circulation during preeclampsia, the mechanisms that link placental ischemia and cardiovascular and renal dysfunction have yet to be fully elucidated. We reported previously that reducing uteroplacental perfusion pressure results in significant and consistent elevations in arterial pressure associated with proteinuria; reductions in renal plasma flow and glomerular filtration rate, an endothelial dysfunction; and intrauterine growth restriction.^3–10

Collectively, these data . . . [Full Text of this Article]