described as pregnancy

The patients homozygous for the D allele, the APF 2 times higher than the enzyme from gomozigot the I allele (12). Polymorphism gene APF and angiotenzinogena poorly connected with the frequency and course of chronic arterial hypertension (HAG) outside pregnancy (7,18,21), but may be risk factor for hypertension in pregnant women (28). Meta-analizom comprising 185 works reliably established that the prevalence of variants of genes renin-angiotenzin-al dosteron (RAAS) depends on the age and race (27). It should be pointed distinct frequency dependence PE of race : White-3 ,71%, blacks-3 ,97%, Amerindians-4 ,81%, Chinese-1 ,44%, the Japanese-1 ,84%, residents Fillipin-2 ,88% (30). Based on the foregoing, it is logical to assume that the PE is hereditary (genetic) defect metabolism defining feature of RAAS, resulting in a lack of activity angiotenzina II, and, as a consequence, to reduce the secretions aldosterone concentration, reduced activity simpatoadrenalovoy system, increase vitality and reduce wandering nerve secreta antidiuretic hormone (ADG). Here it is worth mentioning the results of studies of domestic sponsors of APF activity in normal and complicated pregnancies. It has been shown that the rate of the enzyme in the blood plasma of pregnant constantly growing to trimestru III. The pregnant with advanced PE later, the APF in plasma during the II quarter proved to be significantly below normal. At the same time, pregnant with HAG APF content was significantly higher than normal in all stages of pregnancy (2). System renin-angiotenzin-al dosteron playing a central role in the maintenance of vascular tone and salt and water homeostasis. Normal pregnancy is accompanied by additional income 500-900 mmol of sodium chloride, providing increased plasma fills quickly and substantially increasing vascular bed. The simultaneous increase glomerulyarnoy filtering (up to 50%), accompanied by an enormous number of diesel sodium : up to 30000 mmol / day, with a minimum allocation : 100-200 mmol per day. As a result, pregnant women are especially sensitive to changes in renal sodium reabsorbtsii : when nekompensirovannoy renal excretion rapidly gipovolemiya (23). Insolvency endocrine mechanism replenish and maintain the necessary vnutrisosudistogo fluid volume resulting in the violation during pregnancy, which results in a number of states, usually described as pregnancy (PE) or its complications (VZRP, prematurity). The pregnant women with a defect RAAS lack reabsorbtsii sodium and water (aldosteron, ADG) to the growth of gestatsii growing relative gipovolemiya. Venous vazodilatatsiya streamlined while lowering activity simpatoadrenalovoy system by reducing venous return, also helps to reduce the blood filling the bed, which normally represents about 15% of BCC. When reaching a certain critical value gipovolemii drop in pressure in the blood vessels leading to a reduction in smooth muscle and vazospazmu or even okklyuzii receptacle (1). Vazospazm cause damage endoteliya receptacles, which causes giperaggregatsiyu platelets, reducing product prostatsiklina vascular wall, changing moisture, and ultimately organ failure, I had proteinuriey, human function of the brain and liver. We know that PE in 50-60% of cases by gipoperfuziey marrow (, causing kompensatornuyu reaction dilyatatsii his arteries