alexa [The postanalytical stage of clinical biochemistry. Pathogenetic bases of the classification of arterial hypertension].


Biochemistry & Physiology: Open Access

Author(s): Titov VN

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Abstract A mechanistic model of the cardiovascular system is supposed to provide three variants of an elevation of hydraulic pressure: 1) a reduction in arterial bed volume with unchanged intravascular fluid volume; 2) an increase in intravascular fluid volume without unchanged vascular bed volume; 3) an elevation of blood flow resistance in the system with unchanged volumes of both the system itself and circulating fluid. The first variant includes arterial hypertension (AH) in pheochromocytoma, glucocorticoid hyperproduction, and psychoemotional stress. The second one encompasses AH that develops with excessive dietary intake of NaCl, aldosterone hypersecretion in Conn's syndrome (aldosteroma) and phylogenetically altered right atrial myocytic hyposecretion of atrial natriuretic peptide. The third variant involves all forms of an increase in peripheral blood flow resistance in the arterial bed in aortic coarctation, renovascular hypertension, impaired flow (endothelium)-dependent vasodilation, moderate spasm of muscle-type arterioles, and diseased arterial walls in atherosclerosis--atheromatosis and atherothrombosis. Here there may be an elevation of blood pressure (BP) in erythremia, the effect of leukocyte colony-stimulating factor, and the administration of recombinant erythropoietin. This variant may also include the AH forms that develop during an impaired biological reaction of transcytosis (macropinocytosis) and in the overcoming of bilayer structures by food substrates and humoral mediators at the interface of the common and local intercellular environmental pools: a hematoencephalic form. In impaired transcytosis, there is an encephalopathic form of AH across the blood-brain barrier (an endothelium + astrocyte bilayer), a renal form (an endothelium + podocyte bilayer), pregnant placental AH (an endothelium + trophoblast bilayer), pulmonary AH (an endothelium + pneumocyte bilayer), and AH in atherosclerosis (endothelium + macrophages in the intimal matrix). Normal BP shows the physiological processes of a biological reaction of transcytosis between all the pools of the intercellular environment; no peripheral resistance to blood flow in the arterial bed; normal muscle-type arteriolar function; and physiological processes of metabolism in all paracrine communities of cells in vivo.
This article was published in Klin Lab Diagn and referenced in Biochemistry & Physiology: Open Access

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