[The postanalytical stage of clinical biochemistry. Pathogenetic bases of the classification of arterial hypertension].
TL;DRAbstract
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
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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
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