Figure 1032

Hypertension in preeclampsia. Although the mechanism of the increased blood pressure in preeclampsia is not established, evidence suggests it may involve multiple processes. A possible scenario involves the following: decreased placental production of estrogen and progesterone, both of which have hemodynamic effects; increased circulating endothelial toxins, possibly released from a poorly perfused placenta; and increased activity of the sympathetic nervous system. These processes may then result in alterations in platelet- vascular endothelial cell function, with decrease in vasodilators such as nitric oxide and prostacyclin and increased production of vasoconstrictors such as endothelin (ET). Compensatory suppression of the renin-angiotensin system occurs, suggesting that excess angiotensin II (AII) does not play a major role in preeclamptic hypertension (HT). Finally, sodium retention owing to renal vasoconstriction may further increase blood pressure. cAMP—cyclic adenosine monophosphate; cGMP— cyclic guanosine monophosphate; 5-HT— serotonin; PThr— parathyroid hormone; S2—serotonergic receptors; Thr—thombin TX— thromboxane; TXA2— thromboxane A2. (Adapted from Luscher and Dubey [28]; with permission.)

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