Hypertension in pregnancy includes gestational hypertension, chronic hypertension, preeclampsia, and chronic hypertension. The etiology and pathogenesis doctrine has the causes of insufficient recasting of small uterine spiral arteries, hyperactivation of inflammatory immunity, and damage to vascular endothelial cells. 1. Inadequate remodeling of small uterine spiral arteries: If there is impaired infiltration of extravillous trophoblast cells. This results in “shallow placental attachment” and insufficient filling of the spiral uterine arteries. The diameter of the lumen of the spiral uterine artery is 1/2 of the diameter of the normal artery, and the vascular resistance increases and the perfusion of the placenta decreases. This triggers a series of symptoms of preeclampsia. 2. Inflammatory immune over-activation: in pre-eclampsia, the mother, fetus and the whole body will have excessive inflammatory immune response, resulting in activation of the phenomenon. cd4, cd25 regulatory T cells. CD4 and CD25 regulatory T cells are involved in the regulation of Th1/Th2 immune status. When T cells are reduced, Th1 dominance is generally promoted. Thus maternal immune tolerance to the placenta is reduced. Pre-eclampsia is triggered. 3. Damage to vascular endothelial cells: Vascular endothelial cells reduce the synthesis of vasodilating substances such as nitric oxide and prostacyclin I2. The synthesis of vasodilating substances such as nitric oxide and prostacyclin I2 decreases, while the synthesis of vasoconstricting substances such as endothelin ET and thromboxane A2 increases. This promotes vasospasm. Pregnancy requires regular labor and delivery examinations, and if gestational hypertension develops, medical attention is needed to avoid adverse complications.