Endothelium dependent factors of vasocons triction (thromboxane B2) and vasodilation (6-prostaglandin F1α) in children with primary arterial hypertension
Endothelium dependent factors of vasocons triction (thromboxane B2) and vasodilation (6-prostaglandin F1α) in children with primary arterial hypertension

Summary/Abstract: Background: Vasoconstriction and vasodilatation substance imbalance plays a major role in the formation of arterial hypertension. But the ratio between thromboxane B2 and 6-prostaglandin F1α in children with various forms of primary arterial hypertension (PAH) has been insufficiently studied. Aim of the study: The aim of the study is to explore the features of the content of thromboxane B2, 6-keto-PGF-1alfa and their correlation in children with different clinical and pathogenetic forms of PAH. Material and methods: The study involved 83 children aged 9 to 17. The first group included 32 children with stable PAH, the second – 32 children with labile PAH, the third (control group) – 21 children with normal blood pressure. TXB2 and 6-PGF1α serum levels were investigated by ELISA. All the children also underwent ambulatory blood pressure monitoring (ABPM). Results: The average TXB2 levels in boys were 25.05 ±6.43 ng/ml in the group with stable PAH and 27.26 ±11.26 ng/ml in labile PAH examinees, which exceeded the levels in the control group (p < 0.05). The girls’ TXB2 level was elevated in labile PAH respondents (to 11.06 ±1.79 ng/ml, p < 0.05) and did not differ from the control group with stable PAH. The girls’ 6-PGF1α level was up to 3.41 ±0.52 ng/ml in the stable group of PAH and up to 2.63 ±0.25 ng/ml in the group with labile PAH. Conclusions: The violation of the ratio between endothelial vasoconstriction (thromboxane) and vasodilatation (prostacyclin) factors in boys with PAH is due to increased TXB2 levels compared to children with normal blood pressure (p < 0.05). Girls with PAH reflect better compensatory vasodilatation opportunities compared to boys according to the increased prostacyclin production. The latter prevents the progression of endothelial dysfunction and ensures PAH stabilization in girls.

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