Comparisons of vascular responses to vasoconstrictors in human placenta in preeclampsia between preterm and later term.

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 functions or dysfunction at preterm has not been investigated.
METHODS: Human placenta 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 to angiotensin II, endothelin-1, and other vascular drugs, directly acting on placental arteries 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 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 later term. On the contrary, vascular responses 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 placenta at preterm, and intracellular Ca2+store capacity was damaged too, providing important information on possible contributions of placental vascular dysfunction to pregnant hypertension. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.