Etiology and Risk Factors
Essential hypertension is a multifactorial pathology. The foundation for its development consists of genetically determined defects in cell membranes, which impair the transport of Na^+ and Ca^{2+} ions. This hereditary predisposition has a polygenic nature.
However, genetics serves only as the base. The primary triggering mechanism is prolonged negative psychosocial stress, which exhausts the nervous system and leads to neurosis.
Additional risk factors include:
- Constitution and psyche: asthenic body type, predisposition to depression, hypochondria, and a negative perception of life.
- Lifestyle: sedentary habits (hypodynamia), chronic fatigue, and an excess of dietary sodium (table salt).
- Background conditions: obesity (metabolic syndrome), hypothyroidism, adrenal insufficiency, encephalopathies, and puberty.
Pathogenesis and Hemodynamic Shifts
Chronic stress causes sustained excitation of the sympathetic nuclei in the posterior hypothalamus, adrenergic structures of the reticular formation, and the vasomotor center in the medulla oblongata.
Central activation triggers a powerful humoral response. Biologically active substances with pressor (hypertensive) activity are released into the bloodstream:
- Antidiuretic hormone (ADH / vasopressin);
- Epinephrine (adrenaline);
- Corticosteroids (mineralocorticoids and glucocorticoids);
- Thyroid hormones (T_3 and T_4);
- Endothelin.
Neurogenic and humoral factors jointly increase three key hemodynamic parameters: TPR (total peripheral resistance), circulating blood volume, and cardiac output. The result is a significant spike in blood pressure.
Stages of Disease Progression
The disease progresses in stages, transitioning from temporary fluctuations to irreversible structural changes.
Stage I: Transitory (Stage of Onset) Blood pressure rises intermittently, but temporarily. After an episode of hypertension, pressure can spontaneously return to normal. At this stage, psychosocial and central neurogenic mechanisms predominate. Signs of internal organ (target organ) damage are absent.
Stage II: Stable Hypertension Blood pressure is fixed at a persistently high level. A cascade of morphological changes is triggered:
- Vessels: smooth muscle cells of arterioles undergo hypertrophy, atherosclerosis progresses, and vascular lumens are persistently narrowed.
- Heart: myocardial hypertrophy develops. The "wear-and-tear syndrome of the hypertrophied heart" (cardiomyopathy) emerges, leading to heart failure.
- Kidneys: sclerotic damage leads to the formation of a "primary contracted kidney".
The global pathophysiological outcome of the second stage is ischemia and venous hyperemia of organs, the development of hypoxia (initially circulatory, then mixed), and multiple organ dysfunction syndrome.
Mechanisms of Blood Pressure Stabilization
Four mechanisms ensure the transition of hypertension into a stable form:
- Reflexogenic (baroreceptor): receptors in the aortic arch and carotid sinus "reset" their set point. Afferent depressor impulses to the vasomotor center decrease or cease entirely.
- Endocrine: endocrine glands continuously secrete pressor hormones.
- Metabolic (organ-ischemic): the kidneys play a leading role here. Ischemia of renal tissue stimulates the release of renin. Renin triggers the cascade: angiotensinogen $\rightarrow$ angiotensin I $\rightarrow$ (via ACE) $\rightarrow$ angiotensin II (a potent vasoconstrictor). An excess of hypertensive substances accumulates against a background of deficient hypotensive factors.
- Hemic: chronic tissue hypoxia provokes polycythemia (erythrocytosis). Blood viscosity increases, further raising vascular resistance.
Principles of Therapy
Medical management of arterial hypertension is based on three principles:
- Etiotropic: identification and elimination of the root cause. This includes managing prolonged stress, treating endocrinopathies, and addressing neurogenic disorders.
- Pathogenetic: breaking the vicious cycle of the disease. Therapy aims to reduce cardiac output, TPR, and blood volume, as well as to improve blood rheological properties.
- Symptomatic: improving the patient's quality of life. This involves relieving headaches and depressive episodes, as well as correcting impaired renal and intestinal function.