[Phylogenetic, pathogenetic fundamentals and a role of clinical biochemistry in classification of arterial hypertension].

Classifications of the clinical forms of arterial hypertension (AH) are aimed at differentiating it on etiological grounds; we propose a classification that is based on the common pathogenesis of hydrodynamic pressure elevation in the intravascular pool of the intercellular medium, i.e. arterial blood pressure (BP). We believe that there are only three options for hydrodynamic pressure elevation in a mechanical model of the cardiovascular system: 1) a decrease in the volume of the arterial bed at a constant volume of intravascular fluid; 2) an increase in the volume of intravascular fluid at a constant volume of the vascular bed; and 3) increased blood flow resistance at constant volumes of the vascular bed and intravascular fluid. These options cover all clinical forms of AH in which AP increase is governed by common mechanisms. The first option can be related to AH occurring in pheochromoblastoma, glucocorticoid hyperproduction and psychoemotional stress. The second is associated with AH developing in excessive NaCl consumption with food, increased aldosterone production in Conn's syndrome (primary aldosteronism) and reduced production of atrial natriuretic peptide by phylogenetically modified myocytes of the right atrium. The third option can be linked to all forms of increased peripheral blood flow resistance in the arterial bed occurring in coarctation of the aorta, renovascular hypertension, impaired flow (endothelium)-dependent vasodilation and moderate spasm of muscular arterioles, arterial wall lesion in atherosclerosis, atheromatosis and atherothrombosis, Takayasu syndrome, and obliterating endarteritis. Elevation of BP in erythemia, under the effect of leukocyte colony-stimulating factor and after injection of a recombinant erythropoietin can also be regarded within the frames of the third option. From the viewpoint of general biology, all forms of AH developing against the background of impaired biological function of transcytosis (macropinocytosis) and crossing by food substrates and humoral mediators of bilayer structures between the common and local pools of the intercellular medium, i.e. blood-brain barrier can be referred to as a hematoencephalitic form. Arterial hypertension developing in impaired transcytosis across the blood-brain barrier (endothelium+ astrocytes bilayer), an encephalopathic form; endothelium+ podocytes bilayer, a renal form; endothelium+trophoblasts, placental AH; endothelium +/- pheumocytes, pulmonary AH; and endothelium+intimal macrophages, atherosclerosis-related AH. Normal AP points to: 1) the physiological level of transcytosis between all pools of the intercellular medium; 2) the absence of peripheral blood flow resistance in the arterial bed; 3) normal function of muscle arterioles; and 4) the physiological levels of metabolic processes in all paracrine cell communities in vivo.