Classification of Centrogenic Hypertension
Neurogenic arterial hypertension develops due to dysregulation within central circulatory control mechanisms. Depending on the etiological factor, it is divided into two main groups:
- Due to higher nervous activity (HNA) disorders: Occur against the background of prolonged psychoemotional stress and neuroses. Repeated stress exhausts the adaptive reserves of the nervous system.
- As a result of organic brain lesions: Consequence of traumatic brain injury, tumor growth, encephalitis, or acute cerebrovascular accidents. In this case, regulatory centers are physically damaged or compressed.
Based on the mechanism of origin, these forms are divided into conditioned-reflex (formed on the basis of a conditioned reflex) and unconditioned-reflex (develop in response to a powerful unconditioned stimulus, such as severe pain syndrome or acute renal ischemia).
Pathogenesis: From CNS Activation to Hemodynamic Alterations
The development of sustained hypertension is a multi-step process. It begins with the activation of key central nervous system neurons: sympathetic nuclei of the posterior hypothalamus, adrenergic structures of the reticular formation, and the vasomotor center.
This central activation triggers enhanced hypertensive influences through two pathways:
- Neurogenic pathway: A massive activation of the sympathoadrenal system (SAS) occurs.
- Humoral pathway: Synthesis of hormones with strong pressor effects 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.
Hemodynamically, these processes manifest as a sustained increase in three parameters: arteriolar tone (leading to elevated total peripheral vascular resistance [TPVR]), cardiac output (CO), and circulating blood volume (CBV). The ultimate result is chronically high blood pressure.
Brain Ischemia and Compensatory Hypertension
The body possesses a system to maintain cerebral hemodynamics, protecting the brain from ischemia. It includes three mechanisms: elevation of systemic blood pressure, cerebral vasodilation (reduction of cerebral vascular resistance), and recruitment of collateral circulation. Under physiological conditions, vasodilation predominates because it ensures adequate blood flow without altering hemodynamics in other organs.
However, in prolonged and severe cerebrovascular impairment, a sustained rise in systemic blood pressure develops. This compensatory reaction eventually becomes pathological. Reduced perfusion pressure in cerebral vessels triggers excessive SAS activation and a sustained increase in blood catecholamine concentrations.
Catecholamines exert positive chronotropic and inotropic effects, increasing cardiac output, and constrict arterioles, raising TPVR. In chronic ischemia, the situation is exacerbated by hypercapnia (rising paCO₂). Excess carbon dioxide directly activates neurons of the vasomotor center, increases CNS excitability, and potentiates sympathetic activity, creating a vicious cycle of progressive hypertension.
Conditioned-Reflex Hypertension
This type of pathology develops through repeated pairing of an indifferent (conditioned) signal with the action of hypertensive agents. A conditioned signal might be anticipation of public speaking, a sports competition, or another significant event. The hypertensive agents are typically caffeine, adrenomimetics, psychostimulants, alcohol, or illicit drugs.
After a certain number of such pairings, 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 establishment of chronically elevated blood pressure.
Frequent causes of such states include chronic irritation of extero- and interoreceptors (e.g., during prolonged pain syndromes) and the loss of depressor afferentation—a reduction or complete absence of the physiological inhibitory influence on the tonic activity of the cardiovascular (pressor) center.