Open AccessThe biological reaction of arterial pressure and pathogenesis of programmed arterial hypertension
Author(s) -
В. Н. Титов
Publication year - 2011
Publication title -
arterialʹnaâ gipertenziâ
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.126
H-Index - 5
eISSN - 2411-8524
pISSN - 1607-419X
DOI - 10.18705/1607-419x-2011-17-6-
Subject(s) - nephron , afferent arterioles , endocrinology , medicine , kidney , blood pressure , macula densa , biology , muscle hypertrophy , arterial stiffness , connective tissue , renin–angiotensin system , pathology
Phylogenetically, the following scheme is relevant in vivo: cell → cell community → structural unit of an organ → organ → organ system. A paracrine-regulated cell community is a structural and functional unit of an internal organ; the nephron composed of renal capillary, afferent (efferent) muscular arteriole, and paratubular loose connective tissue is the basic unit of the kidney. In primates the nephron is induced from three germ layers within the first 16 weeks of embryogenesis, which is followed by nephron development during prenatal period; neonephrogenesis does not occur in the postnatal period. Impaired biological function of exotrophy, protein deficiency in mother's diet, and glucocorticoid therapy reduce the number of nephrons, which is reflected by low body weight of the newborn. If a newborn weights less than 2,5 kg, the number of nephrons is so small that they cannot provide the biological function of endoecology in adults without compensatory hypertrophy, which leads to the hydrodynamic pressure elevation in the arterial bed over glomerular filter and increased glomerular filtration. However, hypertrophy is not optimal for compensation of the nephron function. Low body weight at birth and small number of nephrons are risk factors of programmed arterial hypertension in an adult organism.