In:
Current Pharmaceutical Biotechnology, Bentham Science Publishers Ltd., Vol. 21, No. 8 ( 2020-07-08), p. 727-733
Abstract:
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 la ter 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.
Type of Medium:
Online Resource
ISSN:
1389-2010
DOI:
10.2174/1389201021666191217114111
Language:
English
Publisher:
Bentham Science Publishers Ltd.
Publication Date:
2020
SSG:
15,3
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