Lectures in this topical workshop provided insights into the relationships between high blood pressure and metabolic abnormalities and weight abnormalities in adolescents.
Metabolic abnormalities and high blood pressure
Obesity is the major determinant of blood pressure (BP) levels in children and adolescents, as in adults, stated Prof. C. Invitti, Milan, Italy. Central adiposity explains the same proportion of BP levels as generalized adiposity. Prior to the development of glucose intolerance, insulin and glucose levels have a continuous positive and independent relation with BP levels. Uric acid is independently associated with BP in children with normal weight but not in obese children. High nocturnal BP levels are associated with metabolic alterations.
Hyperinsulinemia may be linked to hypertension through several mechanisms, including sodium retention, stimulation of sympathetic system, vascular cell growth, and endothelin, and impairment of endothelial nitric oxide.
In a study of 975 overweight and obese children and adolescents, SBP and DBP increased with increasing levels of insulin. The proportion of children with hypertension was higher in those with abnormal glucose tolerance. The risk of hypertension increased with each unit increase of insulin and glucose levels, adjusted for BMI z score, puberty, age, and sex. A cut-off value of 15.8 mcl/ml had a 64% sensitivity and 59% specificity to identify hypertension, while for 2-hour glucose a cut-off value of 109 mg/ml had a 58% sensitivity and 62% specificity and for fasting glucose a cut-off of 83 mg/ml had a 50% specificity and 64% sensitivity.
Uric acid is an independent predictor of hypertension in adults and shown to be correlated with BP in adolescents. Primary hypertension is associated with hyperuricemia. A small pilot study showed that in 4 of 5 adolescents with hypertension, 1 month of treatment with allopurinol normalized blood pressure. However, it remains unclear whether hyperuricemia is causal or consequential for hypertension.
Adiponectin was shown to be an independent predictor of metabolic syndrome in a study of 162 obese children and adolescents, and there was a tendency for lower SBP with higher levels of adiponectin and a non-significant tendency for increased proportion with isolated systolic hypertension with decreasing levels of adiponectin. Adiponectin was shown to be a marker of endothelial dysfunction in a study of 130 obese children and adolescents.
Birth weight abnormalities and high blood pressure
Lurbe stated that birth weight must be considered when assessing the risk of hypertension. The influence of fetal factors on BP is present early after birth and is modulated by postnatal factors.Current evidence related to the potential intrauterine mechanisms affecting later development of hypertension, the influence of postnatal factors (obesity, salt sensitivity), tracking of BP after birth, and vascular phenotypes of umbilical cords, which may help elucidate the impact of intrauterine life on the development of CV disease, were reviewed by Prof. Lurbe from Valencia, Spain. A complex interplay of genetic and environmental factors affect the development of essential hypertension.
Nilsson and colleagues in 1997 published one of the most important studies regarding the affect of birth weight on BP. In nearly 150,000 persons (18 years old), an inverse relation between low birth weight and higher levels of SBP. A 1996 study showed in children and adolescents without intrauterine growth retardation a positive and significant relation between SBP and current height, weight, and age. Further, the study showed an inverse relation between SBP and birth weight.
The impact of the intrauterine life can be seen by both BP values and changes in BP, and as early as 5 years of age, differences in SBP tracking, with the greatest differences observed at nighttime. An increase of soluble VCAM was associated the higher BP levels.
Possible intrauterine mechanisms include increased fetal glucocorticoid levels, changes in arterial compliance and wall thickness, and glomerular sclerosis leading to a reduction in the number of nephrons. However, the specific mechanisms and their impact and interaction have not been identified to date.
The role of obesity on the development of hypertension has been shown by epidemiological and clinical data. One study has shown that systolic office and ambulatory blood pressure in adolescents increases across four groups stratified by birth weight, adjusted for sex, weight, and height. The highest SBP was found in the lowest birth weight group and 24-hour BP was highest in the lowest birth weight group.
Regarding vascular phenotypes of umbilical cords, research has shown that in the lower birth weight group, endothelial cells from arteries had a reduced intensity of von Willebrand factor, a lower projection area, and a higher cell density at confluence. No significant differences were seen in endothelial cells from the vein or smooth muscle cells.