Neurogenic Arterial Hypertension

Classification of centrogenic hypertension

Neurogenic arterial hypertension develops as a result of a malfunction in the central mechanisms regulating blood circulation. Depending on the etiological factor, it is subdivided into two main groups:

• Due to impaired higher nervous activity (HNA): occurs against the background of prolonged psycho-emotional stress and neuroses. Repeated stress depletes the adaptive reserves of the nervous system.
• As a result of organic brain damage: is a consequence of traumatic brain injury, tumor growth, encephalitis, or acute cerebrovascular accidents. In this case, regulatory centers are physically affected or compressed.

According to the mechanism of onset, such hypertension is divided into conditioned-reflex (formed on the basis of a conditioned reflex) and unconditioned-reflex (develops in response to a powerful unconditioned stimulus, e.g., with severe pain syndrome or acute renal ischemia).

Pathogenesis: from CNS activation to hemodynamic changes

The development of sustained hypertension is a multi-step process. It begins with the activation of key neurons in the central nervous system: the sympathetic nuclei of the posterior hypothalamus, adrenergic structures of the reticular formation, and the vasomotor center.

This central activation triggers an amplification of hypertensive influences in two directions:

1. Neurogenic link: powerful activation of the sympathoadrenal system (SAS) occurs.
2. Humoral link: the synthesis of hormones with pronounced pressor action is stimulated. These include catecholamines, vasopressin (ADH), adrenocorticotropic hormone (ACTH), mineralocorticoids (aldosterone), endothelin, and thyroid hormones. An important role is also played by the increased sensitivity of the heart and vascular wall to these substances.

The hemodynamic realization of these processes consists in a persistent increase in three parameters: arteriole tone (leading to an increase in total peripheral vascular resistance — TPVR), cardiac output (CO), and circulating blood volume (CBV). The result is a stably high blood pressure.

Brain ischemia and compensatory hypertension

There is a system in the body that maintains cerebral hemodynamics, protecting the brain from ischemia. It includes three mechanisms: increased systemic blood pressure, cerebral vasodilation (decreased cerebral vascular resistance), and activation of collateral circulation. Under physiological conditions, vasodilation predominates, as it provides adequate blood flow without altering hemodynamics in other organs.

However, with prolonged and severe cerebrovascular insufficiency, a persistent increase in systemic blood pressure develops. This is a compensatory reaction that transitions into a pathological one. A decrease in perfusion pressure in cerebral vessels causes excessive activation of the SAS and a sustained increase in blood catecholamine concentrations.

Catecholamines exert positive chronotropic and inotropic effects, increasing cardiac output, and constrict arterioles, thereby increasing TPVR. In chronic ischemia, the situation is aggravated by hypercapnia (rising paCO₂). Excess carbon dioxide directly activates neurons of the vasomotor center, increases CNS excitability, and potentiates sympathetic activity, completing the vicious circle of hypertension progression.

Conditioned-reflex hypertension

This type of pathology is formed upon repeated pairing of an indifferent (conditioned) signal with the action of hypertensive agents. The conditioned signal can be information about a public speech, a sports competition, or another significant event. The hypertensive agents are most often caffeine, adrenomimetics, psychostimulants, alcohol, or drugs.

After a certain number of such pairings, the blood pressure elevation occurs in response to the conditioned signal alone, without the actual presence of the chemical stimulus. Over time, this leads to the formation of a persistently elevated blood pressure level.

The most frequent causes for the development of such conditions are chronic irritation of extero- and interoreceptors (e.g., in chronic pain syndromes) and the cessation of depressor afferentation—a decrease or complete absence of the physiological inhibitory influence on the tonic activity of the cardiovascular (pressor) center.

Class and exam questions

What else to study on this topic

• The role of the sympathetic nuclei of the posterior hypothalamus and the reticular formation in blood pressure regulation.
• Mechanisms of formation of unconditioned-reflex hypertension using renal ischemia as an example.
• The effect of endothelin and thyroid hormones on vascular wall tone.
• Pathogenesis of the cessation of depressor afferentation in chronic pain syndromes.
• Differences between mineralocorticoid and glucocorticoid mechanisms of blood pressure elevation.

Other topics in "Chapter 22. Typical Forms of Pathology of the Circulatory System"

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