Pathogenesis of hypertension in overweight and obese patients is to be studied due to the great theoretical and practical importance. The additional mechanisms directly involved in the development of hypertension in subjects with abdominal obesity have been determined. Functional disorders of adipose tissue were shown to play an important role in the development of hypertension in obese patients, and in some cases adiposopathy can be the primary cause of hypertension. Renin-angiotensin-aldosterone system was shown to change signifi cantly in obesity. Understanding the causes and mechanisms of hypertension in patients with abdominal obesity is of particular interest because it allows more focused prevention and treatment of the disease.

The metabolic cardiovascular syndrome (MS) is a common cluster of metabolic abnormalities (abdominal obesity, hypertension, dyslipidemia and carbohydrate metabolism disorders) that are related to insulin resistance and hyperinsulinemia and are associated with accelerated atherogenesis. Insulin excess is known to promote the development of the whole metabolic cascade. Recently it has been shown that the inflammatory and hemostatic abnormalities, immunological disorders, endothelial dysfunction, hyperhomocysteinemia and hyperuricemia are also important features of MS. Despite the numerous studies of MS its underlying cause is still not established. The dysfunction of visceral adipocytes (adiposopathy) might be genetically determined, and is considered nowadays as the main factor contributing to the development of the MS. Understanding the underlying mechanisms is of particular interest for prevention and target therapy of all the components of MS.

Evidence for genetic polymophisms may contribute to the dependence on sex and age differences in biochemical phenotypes, clinical manifestation, severity and success in medical treatment of coronary artery disease (CAD) comes from a variety of studies. Two genetic polymorphisms, L55M and Q192R, in the human antioxidant system paraoxonase 1 gene (PON1) have been shown to be associated with increased risk of CAD. The aim of recent study was to investigate a possible association between polymorphic variants of PON1 and CAD in patients of different age and sex. The group of patients with CAD (323 men and 71 women) and the group of healthy (114 men and 84 women) randomly sampled from St Petersburg were investigated clinically, biochemically and genetically. We found out the genotype L55M and Q192R frequencies in the group of patients with CAD were different depending on sex and age (p = 0,057, p = 0,007). In women with CAD the frequency of 55MM genotype (ОR = 2,1311, 95 % CI 1,14-3,98) was significantly higher and the frequency of 192QR genotype (ОR = 0,59, 95 % CI 0,39-0,89) was significantly lower than in men with CAD who survived myocardial infarction (MI) under the age of 45. Our results suggest that both PON1 polymorphisms play the role in risk of CAD. Furthermore, PON1 polymorphisms act in various ways in patients of different age and sex.