Abstract
The concept of orthostatic hypertension in children was first proposed in 2012. The pathogenesis is not clear by now. Orthostatic hypertension is one of the important causes of orthostatic intolerance in children and is related to the development of essential hypertension in the future. It is commonly seen in older children, with dizziness and syncope as their main clinical manifestations. Non-drug therapy is the commonly used treatment strategy, which is effective to improve the orthostatic intolerance symptoms. In this paper, we reviewed the clinical studies on the pathogenesis, clinical characteristics, diagnostic criteria, and treatment of orthostatic hypertension in children, aiming to provide new insights for the future studies on pediatric orthostatic hypertension.
Highlights
Orthostatic hypertension (OHT) refers to a significant increase in blood pressure (BP) when in the upright position compared to the supine position, and it reflects the abnormal regulation of BP during postural changes
A previous study reported that plasma nitric oxide (NO) levels and nitric oxide synthetase (NOS) activities of children with OHT were significantly lower than those of the control group, and plasma NO levels were negatively correlated with the increases in SBP from supine to upright position
This phenomenon suggests that vascular endothelial injury reflected by NO decrease might participate in the pathogenesis of OHT in children [8]
Summary
Orthostatic hypertension (OHT) refers to a significant increase in blood pressure (BP) when in the upright position compared to the supine position, and it reflects the abnormal regulation of BP during postural changes. A previous study reported that plasma nitric oxide (NO) levels and nitric oxide synthetase (NOS) activities of children with OHT were significantly lower than those of the control group, and plasma NO levels were negatively correlated with the increases in SBP from supine to upright position. This phenomenon suggests that vascular endothelial injury reflected by NO decrease might participate in the pathogenesis of OHT in children [8]. The differences in the mechanisms of pediatric OHT and adult OHT merit further exploration
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