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Figure 1

From: Maternal supraphysiological hypercholesterolemia associates with endothelial dysfunction of the placental microvasculature

Figure 1

Human placental microvascular reactivity. Vascular dilation was determined in venule (□) and arteriole () rings obtained from human placental type I stem villous from pregnancies during which the mother exhibited MPH (white) or MSPH (black). Response to histamine (0.01–1000 μmol/L, 5 min, a), calcitonin gene-related peptide (0.01–1000 nmol/L, CGRP, 5 min, b) or adenosine (0.01–1000 μmol/L, 5 min, c) in vessels pre-incubated with KCl (32.5 mmol/L). The percentage of inhibition of maximal dilation in response to histamine, CGRP and adenosine was determined in the presence of NG-nitro-L-arginine methyl ester (L-NAME, 100 µmol/L, 30 min) in MPH (d) and MSPH (e) venules (white) and arterioles (black). (f) Dilation in response to sodium nitroprusside (10 μmol/L, 5 min) in vessels from MPH (white) or MSPH placentas (black). In (a–c) and (f), the data are expressed as a percentage of maximal dilation in response to KCl. *P < 0.05 versus the MPH values. #P < 0.05 versus the venule values. P < 0.05 versus the CGRP and adenosine values. Values are presented as the mean ± S.E.M. (n = 5–7).

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