Etiology and risk factors
Essential hypertension is a multifactorial pathology. The foundation for its development is genetically determined defects in cell membranes, which disrupt the transport of Na^+ and Ca^{2+} ions. This hereditary predisposition has a polygenic nature.
However, genetics is only the baseline. The main triggering mechanism is prolonged negative psychoemotional stress, which exhausts the nervous system and leads to neurosis.
Additional risk factors:
- Constitution and mental status: asthenic body type, tendency toward depression, hypochondria, and a negative perception of life.
- Lifestyle: physical inactivity, overwork, excess dietary salt (sodium).
- Background conditions: obesity (metabolic syndrome), hypothyroidism, adrenal insufficiency, encephalopathies, and puberty.
Pathogenesis and hemodynamic shifts
Chronic stress causes persistent excitation of the sympathetic nuclei in the posterior hypothalamus, adrenergic structures in the reticular formation, and the vasomotor center in the medulla oblongata.
Central activation triggers a powerful humoral response. Biologically active substances with pressor (hypertensive) action are released into the blood:
- ADH (vasopressin);
- epinephrine;
- corticosteroids (mineralo- and glucocorticoids);
- thyroid hormones (T_3 and T_4);
- endothelin.
Neurogenic and humoral factors jointly increase three key hemodynamic parameters: SVR (systemic vascular resistance), BCC (blood circulation volume), and cardiac output. The result is a significant spike in blood pressure.
Stages of disease development
The disease progresses in stages, moving from temporary disruptions to irreversible structural changes.
Stage I: Transient (onset stage) Blood pressure rises repeatedly but transiently. Following an episode of hypertension, pressure can spontaneously return to normal. At this stage, psychoemotional and central neurogenic mechanisms predominate. Signs of target-organ damage are absent.
Stage II: Stable hypertension Blood pressure stabilizes at a consistently high level. A cascade of morphological changes is triggered:
- Vessels: smooth muscle cells of the arterioles undergo hypertrophy, atherosclerosis progresses, and vascular lumens persistently narrow.
- Heart: myocardial hypertrophy develops. The « hypertrophied heart wear-and-tear complex» (cardiomyopathy) emerges, leading to heart failure.
- Kidneys: due to sclerotic damage, a «primary contracted kidney» forms.
The global pathophysiological outcome of the second stage is ischemia and venous hyperemia of the organs, development of hypoxia (initially circulatory, then mixed), and multiple organ failure.
Mechanisms of blood pressure stabilization
Four mechanisms ensure the transition of hypertension into a stable form:
- Reflectogenic (baroreceptor): receptors of the aortic arch and sinocarotid zone are «reset». Afferent depressor impulses to the vasomotor center decrease or completely cease.
- Endocrine: endocrine glands continuously secrete pressor hormones.
- Metabolic (organ-ischemic): the kidneys play a leading role here. Ischemia of the renal tissue stimulates the release of renin. It triggers the chain: angiotensinogen $\rightarrow$ angiotensin I $\rightarrow$ (with the participation of ACE) $\rightarrow$ angiotensin II (a potent vasoconstrictor). An excess of hypertensive substances forms against the background of a deficiency in hypotensive ones.
- Hemic: chronic tissue hypoxia provokes the development of polycythemia (erythrocytosis). Blood viscosity increases, which further raises vascular resistance.
Principles of therapy
Medical care for arterial hypertension is based on three principles:
- Etiotropic: identifying and eliminating the root cause. Includes combating prolonged stress, treating endocrinopathies and neurogenic disorders.
- Pathogenetic: breaking the vicious cycle of the disease. Therapy aims to reduce cardiac output, SVR, and BCC, as well as improve the rheological properties of the blood.
- Symptomatic: improving the patient's quality of life. Implies stopping headaches and depressive episodes, as well as correcting renal and intestinal dysfunctions.
Briefly: answers to topical questions
What are the groups of symptomatic (secondary) arterial hypertension by etiology?
By etiology, several main groups of secondary (symptomatic) arterial hypertension are distinguished.
- Renal — associated with renal parenchyma diseases (renoparenchymal) or vascular pathology (renovascular).
- Endocrine — caused by pathology of the endocrine glands (adrenal, pituitary, thyroid, and parathyroid).
- Neurogenic — centrogenic forms associated with brain diseases, trauma, inflammation, or polyneuritis.
- Cardiovascular (hemodynamic) — occur in aortic pathology, heart defects, and systemic hemodynamic disorders.
- Drug-induced — develop with the use of glucocorticoids, nonsteroidal anti-inflammatory drugs, adrenomimetics, and other medications.
The classification also includes gestational and postoperative hypertension, as well as forms associated with obstructive sleep apnea syndrome.
What stages of essential hypertension are distinguished according to the WHO classification depending on target-organ damage?
In the sources, the WHO classification (1962) is not given in full; only the initial stage is described in detail.
- Stage I — characterized by an increase in blood pressure above 160/95 mm Hg. A key sign of this stage is the absence of organic changes in the cardiovascular system and target organs.
At the same time, the materials describe the general morphological stages of essential hypertension:
- Stage I (transient) — signs of internal organ damage are absent.
- Stage II (stable hypertension) — stabilization of blood pressure at an elevated level, cardiac hypertrophy, nephrosclerosis, and atherosclerosis.
- Stage III (organic) — development of vascular catastrophes, gross organic changes, multiple organ failure, and the formation of a primarily contracted kidney.
What are the main groups of pharmacological agents used for pathogenetic therapy of essential hypertension?
For the pathogenetic therapy of arterial hypertension, the materials indicate antihypertensive drugs aimed at blocking or reducing the effectiveness of key links in the pathogenesis.
Main drug classes:
- ACE inhibitors — enalapril, perindopril, etc.
- Angiotensin II receptor blockers (ARBs) — losartan, valsartan, olmesartan.
- Calcium channel blockers.
- Beta-blockers.
- Diuretics; thiazide diuretics are indicated as drugs of choice for monotherapy in the early stages of essential hypertension, whereas in combination therapy, diuretics counteract fluid and electrolyte retention.
Additional drug classes:
- Imidazoline receptor agonists.
- Alpha-blockers.
- Direct renin inhibitors — aliskiren.
Centrally acting antihypertensive drugs are also described: they suppress central sympathetic impulses directed to the heart and blood vessels.
For quick memorization of the four mechanisms of BP stabilization, use the acronym REM(G): Reflexogenic, Endocrine, Metabolic (organ-ischemic), Hhemic.
Class and exam questions
Is hypertension always an independent disease?
No, secondary (symptomatic) arterial hypertension exists. For example, renovascular hypertension develops when renal artery blood flow is impaired (in 60–70% of cases due to atherosclerosis), while renoparenchymal hypertension develops in glomerulonephritis.
How does the first stage of essential hypertension differ from the second?
In the first (transitory) stage, the blood pressure elevation is transient, and target organs are not damaged. In the second stage, hypertension becomes stable, and myocardial hypertrophy, nephrosclerosis, and atherosclerosis develop.
What is the "wear-and-tear complex of the hypertrophied heart"?
This is a specific cardiomyopathy that occurs during the stage of stable hypertension. It develops due to a disruption in the balanced growth of myocardial structures under conditions of constant hemodynamic overload.
What else to study on this topic
- The role of the renin-angiotensin system (RAS) in the regulation of vascular tone
- Pathogenesis of secondary arterial hypertension (renoparenchymal and renovascular)
- Mechanisms of multi-organ failure in stable hypertension
- Types of arterial hypotension and the pathophysiology of shock (vasodilatory, cardiogenic, hypovolcemic)
Master the entire topic in the "Pathophysiology" course
This is a summary. The course covers everything tested in classes and exams.
- Complete study guide on "Essential Hypertension" and 4,913 other pages for this subject
- Assignments and quizzes after every topic — just like in a colloquium
- AI tutor answers questions on the topic anytime
- 135 video lessons on the subject
Other topics in "Chapter 22. Typical Forms of Pathology of the Circulatory System"
Free video lessons: pathophysiologyShort lessons with lecture notes — no registration required.
Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.