What causes arterial hypertension (hypertension)?

The factors that determine the level of blood pressure in children are varied and can be conditionally divided into endogenous (heredity, body weight, height, personality traits) and exogenous (diet, physical inactivity, psycho-emotional stress).

Hereditary predisposition

The following facts indicate the importance of heredity in the pathogenesis of arterial hypertension:

• high correlation of blood pressure in monozygotic twins compared to dizygotic twins;
• higher blood pressure values in children with a family history of hypertension.

The genes responsible for the development of hypertension have not yet been discovered. The greatest progress in understanding the role of hereditary predisposition to arterial hypertension has been achieved in studying the genes of the renin-angiotensin system.

The angiotensinogen molecule determines the level of angiotensin I. The participation of the angiotensin gene in the formation of the renin-angiotensin-aldosterone system profile has been determined. The angiotensinogen gene is located on chromosome 1.

The ACE gene product determines the formation of angiotensin II from angiotensin I. The ACE gene can be represented by long and short alleles: the so-called Insertion/Deletion polymorphism. The DD genotype is considered an independent risk factor for the development of essential hypertension. The highest level of ACE gene expression is characteristic of the endothelium of small muscular arteries and arterioles. ACE gene expression is sharply increased in suddenly deceased patients with arterial hypertension.

The polygenic nature of inheritance of arterial hypertension is currently recognized. The following facts support this:

• high prevalence of arterial hypertension in children in families with persistently high blood pressure;
• elevated blood pressure and a higher risk of developing hypertension in members of the same family if there are three or more people with arterial hypertension;
• 3-4 times higher frequency of stable arterial hypertension among siblings (brother or sister of the patient) and parents of probands (patients) compared to the population;
• clinical polymorphism of arterial hypertension in children and adolescents;
• higher incidence of arterial hypertension among siblings of boys, more severe course of the disease with crisis conditions;
• 2-3 times higher concordance for hypertension in monozygotic twins compared to dizygotic twins;
• dependence of the risk of a sibling's disease on the age at which the proband became ill (the earlier the disease manifested itself in the proband, the higher the risk for the sibling);
• high probability of high blood pressure in prepubertal age in the presence of arterial hypertension in both parents.

A connection between arterial hypertension and the carriage of the HLA AH and B22 tissue compatibility genes was revealed. Data were obtained indicating that genetic factors determine up to 38% of the phenotypic variability of systolic blood pressure and up to 42% of diastolic blood pressure. Environmental factors make a significant contribution to maintaining the optimal level of diastolic and systolic blood pressure.

Genetic factors do not always lead to the development of hypertension. The influence of genes on blood pressure is significantly modified by such factors as stress, consumption of table salt and alcohol, obesity, and low physical activity. Moreover, at the level of cells and tissues, the prohypertensive effects of genetic factors can be weakened by physiological mechanisms that ensure stability of blood pressure (kallikrein-kinin system).

Consumption of table salt

Consumption of table salt is one of the main exogenous factors affecting blood pressure. In populations where less salt is consumed, a less significant increase in blood pressure with age and lower average values are noted compared to populations where more table salt is consumed. It has been suggested that hypertension is humanity's retribution for excessive consumption of table salt, which the kidneys are unable to excrete. The body's regulatory systems increase systemic arterial pressure in order to increase the excretion of sodium ions consumed with food in excessive quantities by increasing the pressure in the renal arteries.

In individuals predisposed to the development of hypertension, autoregulation of renal blood flow and glomerular filtration, which is normally controlled by the juxtaglomerular apparatus, is impaired. With an increase in the flow of chloride ions into the distal tubules in the area of the macula densa, the resistance of the afferent arterioles decreases. This leads to an increase in the rate of glomerular filtration and, ultimately, to an increase in the excretion of excess sodium and chloride ions from the body. Impairment of the tubuloglomerular mechanism of autoregulation of renal circulation leads to the fact that sodium chloride is retained in the body and contributes to an increase in arterial pressure. Impaired renal excretion of sodium in patients with hypertension may be a consequence of a hereditary defect in ion transport through the epithelial cells of the renal tubules. To prevent sodium retention in the body, systemic arterial pressure and, consequently, renal perfusion arterial pressure increase.

Sensitivity to salt load is related to genetically determined features. The connection between arterial hypertension and sodium metabolism is known. Increased intracellular sodium level reflects a high risk of developing arterial hypertension.

Overweight

Almost all epidemiological studies have found a close relationship between blood pressure and body weight. People with higher body weight have significantly higher blood pressure values compared to people with normal weight.

Excess body weight is a common phenomenon in the child population. In a survey of schoolchildren aged 7-17, individuals with excess body weight accounted for 25.8%. In the American population, body weight 29% higher than ideal was found in 15.6% of children aged 10-15. There is a tendency for the prevalence of excess body weight to increase with age. Thus, if at 6 years of age, body weight exceeding ideal by 20% occurs in 2% of children, then by 14-18 years - in 5%. The coefficient of stability of body weight indicators during dynamic observation for 6 years is 0.6-0.8. Consequently, body weight control in children is the basis for preventing obesity in adults. Weight loss is accompanied by a decrease in blood pressure.

Half of overweight children have elevated systolic and diastolic blood pressure. Excess body weight is associated with elevated plasma triglyceride levels and decreased high-density lipoprotein cholesterol, elevated fasting glucose and immunoreactive insulin levels in the blood, and decreased glucose tolerance. The term "metabolic hypertension" or "metabolic quartet" is used to combine these indicators with arterial hypertension. Insufficient insulin receptors in cell membranes are a genetic cause of hyperinsulinemia, hyperglycemia, and dyslipidemia, as well as a significant risk factor for arterial hypertension and obesity. The main pathogenetic mechanism of the "metabolic quartet" syndrome is low glucose assimilation by the cell. In these patients, metabolic disorders combined with dyslipidemia contribute to the early and accelerated development of atherosclerosis.

The incidence of overweight is influenced by insufficient levels of physical activity.

To identify children with excess body weight, the thickness of the skin fold on the shoulder, abdomen, and the Quetelet, Cole, and other weight-height indices are used. Children with Quetelet index values exceeding the 90th percentile of the distribution curve (Appendix 3) are considered to have excess body weight.

However, not only excess weight, but also low body weight is associated with elevated blood pressure. Thus, in a 5-year study of children with blood pressure above the 95th percentile, the highest coefficient of stability of elevated DBP was observed in the subgroup of children with low body weight. Birth weight also affects blood pressure. Low birth weight is associated with increases in blood pressure in adolescence.

Psycho-emotional stress

For a long time, the mechanisms of hypertension development were explained from the position of the neurogenic theory of G.F. Lang and A.L. Myasnikov. The basis of this theory is the concept of central dysregulation of the autonomic nervous system with increased activity of the sympathoadrenal link. At present, there is a significant amount of clinical and experimental data confirming that psychoemotional factors are of great importance in the occurrence and course of arterial hypertension.

Increased emotional sensitivity and vulnerability lead to the development of maladaptation syndrome. The effect of a stressor is refracted through an assessment of its impact on the individual and depends on characterological features and dominant motives of activity. The occurrence of emotional tension is determined not by the absolute strength of the stressor, but by the teenager's social and personal attitude towards it.

In a stressful situation, social support (friends, parents, relatives) is of great importance for the development or absence of arterial hypertension. In its absence, the stressful situation worsens, which is associated with increases in blood pressure, especially DBP.

During psychoemotional stress, irritation is first perceived by sensory receptors, the impulse goes to the hypothalamic structures of the brain, which serve as both the vegetative and emotional center responsible for the activation of the sympathetic nervous system. In the second, neurohumoral, phase, humoral links are included in providing psychoemotional stress, the main ones being the pituitary-adrenal system and the renin-angiotensin system. At the level of the hypothalamic-reticular structures, the so-called stagnant focus of excitation is formed. Psychoemotional stress is accompanied by both psychological and vegetative manifestations. Activation of the sympathoadrenal system is a non-specific component of the adaptive reaction and does not serve as the leading factor in the pressor reaction. In this case, the manifestation of cardiovascular hyperreactivity with an increase in total peripheral vascular resistance is of greater importance.

Different degrees of resistance to stress were found, resistant and stress-prone groups were identified, and the latter could not adapt to the stressful situation and died from acute heart failure with massive necrosis in the myocardium. The resistance of the cardiovascular system to stress is largely determined genetically and is determined by the selective distribution of biogenic amines, the ratio of adrenoreceptors, cholinergic and serotonergic mediator systems in brain structures, as well as the sensitivity of adrenoreceptors to catecholamines.