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.
Sphingosine-1-Phosphate Induces Pulmonary Vascular Inflammation by Activating the Canonical NF-κB and Inflammasome Pathway
