Abstract

Background: Placental blood vessels play important roles in maternal-fetal circulation. Although pathologic mechanisms of preeclampsia are unclear, it is known that placental vascular dysfunction could contribute to pregnant hypertension. However, placental micro-vessel function or dysfunction at preterm has not been investigated.

Methods: Human placentas from normal and preeclamptic pregnancies at preterm and term were obtained. Placental micro-vessels were used for determining vascular tension and responses to various vasoconstrictors as well as intracellular calcium store capability. It was the first time to show vascular responses in placental arteries to angiotensin II, endothelin-1, and other vascular drugs at preterm.

Results: Compared to the control, placental vascular contractile responses to angiotensin II and caffeine were significantly decreased, while placental vascular responses to KCl, endothelin-1, and bradykinin were not significantly altered in the later term group in preeclampsia. In comparison of placental micro-vessel tension between the preterm and later term, caffeine- and serotonin-induced vascular contractions were significantly weaker in the preterm than that in the later term. On the contrary, vascular response to angiotensin II was increased in the preterm preeclampsia, while KCl-, endothelin-1, and bradykinin-mediated placental vessel responses in the preterm preeclampsia were similar to that in later term preeclampsia.

Conclusion: New data showed that micro-vessel responses to angiotensin II and serotonin, not endothelin- 1 or bradykinin, were significantly reduced in the human placentas at preterm, and intracellular Ca2+ store capacity was damaged too, providing important information on possible contributions of placental vascular dysfunction to pregnant hypertension.

Keywords: Preeclampsia, placental vessel, vasoconstriction, preterm, serotonin, human umbilical cord.

Graphical Abstract