What causes arterial hypertension (hypertension)?

Factors determining the level of blood pressure in children are diverse, they can be conventionally divided into endogenous (heredity, body weight, height, personality characteristics) and exogenous (diet, hypodynamia, psychoemotional stress).

Hereditary predisposition

The following facts indicate the significance of heredity in the pathogenesis of hypertension:

• high correlation of arterial pressure in monozygotic twins as compared with dizygotic twins;
• higher values of blood pressure in children with a hereditary burden of hypertension.

Until the genes responsible for the onset of hypertension have been found. The greatest progress in understanding the role of hereditary predisposition to arterial hypertension was achieved in the study of 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 profile of the renin-angiotensin-aldosterone system has been determined. The gene of angiotensinogen is located on chromosome 1.

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

At present, the polygenic nature of inheritance of arterial hypertension is recognized. The following facts support this:

• high prevalence of arterial hypertension in children in families with persistent increase in blood pressure;
• an increased level of blood pressure and a greater risk of developing hypertension in members of the same family in the presence of three or more people with hypertension;
• 3-4 times higher frequency of stable arterial hypertension among siblings (brother or sister of the patient) and parents of probands (patients) compared with the population;
• clinical polymorphism of arterial hypertension in children and adolescents;
• a high incidence of arterial hypertension among boys' sibs, a more severe course of the disease with crisis conditions;
• 2-3 times higher concordance in hypertensive disease in monozygotic twins compared with dizygotic;
• the dependence of the risk of Sibs disease on the age at which the proband was ill (the earlier the disease appeared in the proband, the higher the risk for sibs);
• a high probability of increasing blood pressure in prepubertal age in the presence of hypertension in both parents.

The connection of arterial hypertension with the carrier of genes of tissue compatibility of HLA AN and B22 has been revealed. Data have been obtained indicating that genetic factors determine up to 38% of phenotypic variability in systolic blood pressure and up to 42% of diastolic blood pressure. A significant contribution to maintaining the optimal level of diastolic and systolic blood pressure is made by environmental factors.

Genetic factors do not always lead to the development of hypertension. The influence of genes on the level of blood pressure is largely modified by factors such as stress, consumption of table salt and alcohol, obesity, 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 the stability of the level of arterial pressure (kallikrein-kinin system).

Consumption of table salt

Consumption of table salt is one of the main exogenous factors. Affecting the level of blood pressure. In populations where food is consumed less salt. Note a less significant increase in blood pressure levels with age and lower average values compared with populations that consume more salt. It is suggested that hypertensive disease is the payment of humanity for excessive consumption of table salt, which the kidneys are not able to withdraw. Regulatory body systems increase systemic arterial pressure to increase the excretion of sodium ions consumed with food in excessive amounts by increasing the pressure in the renal arteries.

People who are predisposed to the development of hypertensive disease have disrupted autoregulation of renal blood flow and glomerular filtration, which is normally controlled by the juxtaglomerular apparatus. With an increase in the intake of chloride ions into the distal tubules, the resistance of the afferent arterioles decreases in the region of the dense spot. This leads to an increase in the glomerular filtration rate and, ultimately, an increase in the excretion of excess sodium and chlorine ions from the body. Violation of the tubulohlomerular mechanism of autoregulation of the renal circulation leads to the fact that sodium chloride is retained in the body and promotes an increase in blood pressure. Violation of renal sodium excretion in patients with essential hypertension can be a consequence of the hereditary defect of ion transport through the epithelial cells of the renal tubules. To prevent sodium retention in the body, there is an increase in systemic arterial pressure and, consequently, renal perfusion blood pressure.

Sensitivity to salt load refers to genetically determined characteristics. The connection of arterial hypertension with the metabolism of sodium is known. The increased level of intracellular sodium reflects a high risk of hypertension.

Excess body weight

Almost all epidemiological studies have revealed a close relationship between the level of blood pressure and body weight. In individuals with a higher body weight, blood pressure values are significantly higher than those with normal weight.

Excess body weight is a common phenomenon in the child population. At examination of schoolchildren of 7-17 years of age persons with excess weight of the body made 25.8%. In the American population, body weight was 29% higher than the ideal body weight in 15.6% of children aged 10-15 years. There was a tendency to increase the prevalence of overweight with age. So, if at 6 years, body weight exceeding the ideal by 20%, occurs in 2% of children, then by 14-18 years - in 5%. The coefficient of stability of body weight during dynamic observation for 6 years is 0.6-0.8. Therefore, the control of body weight in children is the basis for preventing the development of obesity in adults. Decreased body weight is accompanied by a decrease in blood pressure.

Half of children with overweight have an increased systolic and diastolic blood pressure. Excess body weight is associated with an increased plasma level of triglycerides and a decrease in high-density lipoprotein cholesterol, increased fasting glucose and immuno-reactive insulin in the blood, and a decrease in glucose tolerance. To combine these indicators with arterial hypertension, the term "metabolic variant of hypertension" is used. Or the "metabolic quartet". Insulin receptor insufficiency of cell membranes is the genetic cause of hyperinsulinemia, hyperglycemia and dyslipidemia, as well as a significant risk factor for hypertension and obesity. The main pathogenetic mechanism of the syndrome of the "metabolic quartet" is a low assimilation of glucose by the cell. In these patients, metabolic disorders in combination with dyslipidemia contribute to the early and accelerated development of atherosclerosis.

The frequency of overweight is affected by inadequate physical activity.

To detect children with excessive body weight, the thickness of the skin fold on the shoulder, abdomen, mass-growth indices of Quetelet is used. Cole et al. It is believed that children with a Quetelet index value exceeding the 90th percentile of the distribution curve (Appendix 3) have an excess body weight.

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

Psychoemotional stress

For a long time, the mechanisms of the development of hypertension 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 vegetative department of the nervous system with an increase in the activity of the sympathoadrenal link. At present, there is a significant amount of clinical and experimental data confirming that psychoemotional factors play a significant role in the onset and course of hypertension.

Increased emotional sensitivity, vulnerability lead to the development of the syndrome of disadaptation. The action of the stressor is refracted through an assessment of its impact on the individual and depends on the characteristics of the character, the dominant motives of the activity. The emergence of emotional stress is determined not by the absolute strength of the stressor, but by the social-personal attitude of the adolescent to him.

In a stressful situation, social support (friends, parents, loved ones) is very important for the development or absence of hypertension. In its absence, the stressful situation is exacerbated, which is associated with an increase in blood pressure, mostly DBP.

With psychoemotional stress, irritation is first perceived by sensitive receptors, the impulse arrives at the hypothalamic brain structures that serve as the vegetative and emotional center responsible for the activation of the sympathetic nervous system. In the second, neurohumoral phase, humoral links are included in the provision of psychoemotional stress, the main ones of which are the pituitary-adrenal and renin-angiotensin system. At the level of the hypothalamic-reticular structures, a so-called stagnant foci of excitation is formed. Psychoemotional tension is accompanied by both psychological and vegetative manifestations. Activation of the sympathoadrenal system is a nonspecific component of the adaptation reaction and does not serve as a leading factor in the pressor response. In this case, the manifestation of cardiovascular hyperreactivity with increasing total peripheral vascular resistance is of greater importance.

A different degree of resistance to stress was found, stable and predisposed to stress 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. Stability of the cardiovascular system to stress is largely determined genetically and is determined by the selective distribution of biogenic amines, the ratio of adreno, cholino and serotonergic mediator systems in the brain structures, and also the sensitivity of adrenoreceptors to catecholamines.