부산대학교 도서관

Pediatric pre-hypertension (pre-HTN) has a complex multifactorial etiology. Although most cases are secondary to other disorders, a substantial number of children and adolescents have primary or essential HTN and pre-HTN. The gene-gene and gene-environment interactions should be considered in this context. The strong relationship of pre-HTN with environmental factors such as air pollution, noise pollution and passive smoking and obesity suggest that its prevalence will be escalating. Exposure to ambient particulate matters may increase blood pressure (BP) within hours to days. The underlying biologic pathways include autonomic nervous system imbalance and arterial vascular dysfunction or vasoconstriction because of systemic oxidative stress and inflammation. Likewise, tobacco smoke exposure of pregnant mothers increases systolic BP of their offspring in early infancy. Parental smoking also independently affects systolic BP among healthy preschool children. Noise exposure, notably in night, is associated with catecholamine secretion, increased BP and a pre- HTN state even in pre-school age children. Excess weight is associated with dysfunction of the adipose tissue, consisting of enlarged hypertrophied adipocytes, increased infiltration by macrophages and variations in secretion of adipokines and free fatty acids. These changes would result in chronic vascular inflammation, oxidative stress, activation of the renin-angiotensin-aldosterone system and sympathetic response, and ultimately to pre-HTN from childhood. Prevention and control of the modifiable risk factors of pre-HTN from prenatal period can have long-term health impact on primordial and primary prevention of chronic non-communicable diseases. This review presents a general view on the diagnosis, prevalence and etiology of pre-HTN along with practical measures for its prevention and control. [ABSTRACT FROM AUTHOR]