Humankind ponders mystery pre-eclampsia in ancient times. Man -edinstvennoe animal on the planet, who described the disease. Two-thirds of all pregnant women with PE are young healthy women pervoberemennye nevertheless perinatal mortality when the disease is growing 20 times. None of the many theories about the origin of PE is not allowed to develop reliable methods for its prevention, because they were only consequence of the disease, without revealing its true causes. This article presents an original view of the hypertension in pregnant women, which is seen as a compensatory reaction in response to changes in the pregnancy of the circulatory system, the fundamental bases of all complex organisms. Over the past decade, there are strong evidence of hereditary nature of PE. In regions of chromosomes 7q36 and 2r13 found lokusy responsible for the family inheritance hypertension pregnant and for the development of PE (4,5). It has been determined that there are genotypes angiotenzinogena : M (metionin) 235 and T (treonin) 235. Gomozigoty code T235 in PE occur much more frequently : 87-92%, compared with the control : 56% (22). We detected the presence of mutations in the amino acid composition angiotenzinogena : Replacing leytsina at fenilalanin in his position 10-meste splitting reninom. Mutation significantly alter interaction with angiotenzinogena reninom and angiotenzinprevraschayu Attraction enzyme (ACE) that could lead to the development of PE beremennyh-nositeley mutations (16). The pregnant with PE revealed declining concentration and activity angiotenzina and aldosterone concentration in the same total renin and angiotenzinogena and hypersensitivity to injecting angiotenzinu (9). In recent years, opened the ACE gene variants related to the presence of I-allel, or lack-allel D, introne 16 ACE gene insertion of 287 nucleotides.
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