Etiology and key development theories
Hypertensive disease is a multifactorial pathology. Its occurrence is caused by a complex combination of genetic predisposition and negative environmental impacts. Modern pathological anatomy distinguishes three main theories of etiology:
- Neurogenic theory (G.F. Lang, A.L. Myasnikov): a leading role is assigned to chronic psycho-emotional overstrain, frequent stress, conflicts, and prolonged attention span tension.
- Theory of renal-volume regulation (A. Guyton): based on a hereditary defect in the mechanisms of blood pressure control by the kidneys.
- Membrane theory (Yu.V. Postnov, S.N. Orlov): genetically determined breakdown of ion pumps in cell membranes leads to impaired intracellular metabolism of calcium and sodium ions.
The disease has a polygenic inheritance and a familial character. Among significant risk factors, alimentary factors (excess dietary salt against a background of potassium, calcium, and magnesium deficiency), constitutional factors (excess body weight), as well as occupational hazards (constant noise, vibration, the need to suppress negative emotions, which is especially characteristic of doctors and teachers) are distinguished.
Neurogenic pathogenesis and stages of dysregulation
According to the concept of P.K. Anokhin, G.F. Lang, and A.L. Myasnikov, the triggering mechanism is prolonged stress. It reduces the inhibitory effect of the cerebral cortex on subcortical structures. As a result, a congestive focus of excitation is formed in the hypothalamo-pituitary system. This causes persistent overexcitation of pressor autonomic centers, impaired protein and fat metabolism, and, consequently, arteriolar spasm.
The process of blood pressure regulation disorder goes through two key stages:
- Initial stage (compensation): the primary increase in pressure is detected by baroreceptors of the carotid sinus zone and aortic arch. They stimulate the vasomotor center of the medulla oblongata, which temporarily returns the parameters to normal.
- Progression (failure of adaptation): with incessant stress, the load on baroreceptors increases, and they become depleted. Central regulation is disrupted, and the sympathoadrenal system (SAS) is actively involved in the process. An excess of catecholamines is released into the blood, which provokes an additional and already persistent rise in pressure.
Hemodynamic mechanisms
The main hemodynamic cause of hypertensive disease is an inadequate increase in total peripheral vascular resistance. The tone of peripheral arterioles increases under the action of several factors:
- Vascular wall edema: water and sodium ion retention causes a "soaking effect," narrowing the vessel lumen and increasing its sensitivity to vasoconstrictors.
- Direct vasoconstriction: the effect of pressor agents such as angiotensin II, cortisol, prostaglandin F2α, and cyclic guanosine monophosphate (cGMP).
- Ionic factor: the accumulation of calcium (Ca2+) inside the smooth muscle cells of arterioles stimulates their contraction.
- Deficit of vasodilators: a drop in the synthesis of depressor substances (prostaglandins E, A, D, prostacyclin, and bradykinin).
Renal factor and the vicious circle of hypervolemia
Spasm of renal arterioles in combination with sympathetic influences activates the juxtaglomerular apparatus. The renin-angiotensin-aldosterone system (RAAS) is triggered, which further enhances vasoconstriction. With high RAAS activity, vasoconstrictor hypertension develops; with low activity, hypervolemic hypertension develops.
In parallel, the renal-volume mechanism is switched on. In response to a rise in pressure, the kidneys reduce sodium excretion. Water and sodium retention occurs, and the volume of blood plasma and interstitial fluid increases (hypervolemia). This leads to an increase in venous return and cardiac output.
A vicious circle is formed: the increase in plasma volume stimulates the secretion of natriuretic hormone. Attempting to compensate for hypervolemia, the hormone inhibits sodium-potassium ATPase to enhance renal sodium excretion. However, this mechanism acts systemically: sodium and water are retained in erythrocytes and arteriolar walls. As a result, vascular resistance paradoxically increases, and blood pressure continues to rise.
Briefly: answers to topical questions
How does the renin-angiotensin-aldosterone system (RAAS) function in hypertensive disease?
In hypertensive disease, the functioning of the renin-angiotensin-aldosterone system (RAAS) determines the mechanism of blood pressure elevation. High RAAS activity leads to the development of vasoconstrictor hypertension due to increased arteriolar spasm (including intrarenal arteries). Low activity of the system contributes to the development of hypervolemic hypertension. In the malignant course, hyperreninemia causes generalized vasospasm, a sharp increase in blood pressure, and necrosis of the vessels of the kidneys and other organs.
What are the clinical and morphological forms of hypertensive disease?
Benign and malignant clinical and morphological forms of hypertensive disease are distinguished, as well as hypertensive crisis.
- Benign form is characterized by a prolonged and gradual increase in blood pressure.
- Malignant form is distinguished by rapid progression, frequent crises, and diastolic pressure above 120 mm Hg. The morphological basis is fibrinoid necrosis of arterioles and the formation of aneurysms of their walls.
- Hypertensive crisis is manifested by a rapid and high rise in blood pressure.
The renal form of benign hypertensive disease is also mentioned.
Which organs are classified as "target organs" in hypertensive disease?
The "target organs" in hypertensive disease include the heart, kidneys, brain, and fundus vessels. The presence of objective changes in these organs is a key sign for staging the disease. In stage II, the function of target organs is not impaired, while in stage III, impairment of their functions is diagnosed (for example, heart or renal failure, vascular catastrophes).
What morphological changes develop in the kidneys in benign hypertensive disease?
In benign hypertensive disease, arteriolosclerotic nephrosclerosis (primary contracted kidney) develops in the kidneys. Macroscopically, the kidneys are usually normal in size or moderately reduced (weight up to 110–130 g), deformed, and their surface acquires a fine-grained appearance. The microscopic picture includes:
- Hyalinosis of the walls of afferent arterioles and glomeruli.
- Glomerulosclerosis with the loss of a portion of nephrons.
- Sclerosis and lymphocytic infiltration of the stroma.
- **Tubular epithelial atrophy.
To memorize the main pressor agents causing direct vasoconstriction, use the abbreviation KAPC (CAPC): Kortisol (Cortisol), Angiotensin II, Prostaglandin F2α, CGMP (cGMP).
Class and exam questions
How does hypertension differ from symptomatic arterial hypertension?
Symptomatic (secondary) hypertension is merely a sign of another disease and completely disappears after its cure. Essential hypertension is an independent primary pathology with an unknown exact cause, accounting for up to 95% of all cases.
How does natriuretic peptide affect blood vessels in hypertension?
Trying to reduce the circulating blood volume, it blocks sodium-potassium ATPase. This leads to the retention of sodium and water in the arteriolar walls, which causes their edema and paradoxically increases total peripheral vascular resistance.
What is the role of cell membranes in the pathogenesis of the disease?
Due to a genetic defect in ion pumps, calcium and sodium ions accumulate in cells (including myocytes). This makes vascular smooth muscle cells hypersensitive to vasoconstrictor neurotransmitters and humoral factors.
What else to study on this topic
- The role of the renin-angiotensin-aldosterone system (RAAS) in the regulation of vascular tone
- Mechanisms of depletion of depressor systems (prostaglandins, bradykinin)
- Pathogenesis of hypervolemic and vasoconstrictor forms of arterial hypertension
- Effect of electrolyte imbalance (sodium, potassium, calcium, magnesium) on blood pressure levels
- Relationship between sympathoadrenal system activity and baroreceptor exhaustion
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