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Oxidative stress can modulate blood pressure levels in different models. Xanthine oxidoreductase is one of the enzymes producing free radicals in the cardiovascular system, and it can contribute to the increment of the oxidative stress and, consequently, blood pressure. We analyzed the association between the -337GA and 565+64CT polymorphisms of the xanthine oxidoreductase gene with blood pressure and oxidative stress levels.These polymorphisms were studied in a case-control study (185 patients with hypertension and 385 normotensive controls), we found that these polymorphisms were related to blood pressure levels. This association was high in patients with hypertension and showed an additive effect but did not increase the risk of developing hypertension. We studied an additional and independent sample of patients with hypertension (n=100) to know the association of these polymorphisms with oxidative stress levels.We found that these polymorphisms were related to blood pressure levels. This association was high in hypertensive patients and showed an additive effect, but does not increase the risk of developing hypertension. We have found that the same alleles related with higher blood pressure-337A and 565+64C were related with increased oxidative stress in patients with hypertension.Our results suggest that polymorphisms -337GA and 565+64CT of xanthine oxidoreductase gene are related with blood pressure and oxidative stress in hypertension, adding evidence to the role of xanthine oxidoreductase and oxidative stress in blood pressure. [ABSTRACT FROM AUTHOR]

Familial hypercholesterolaemia (FH) is an autosomal dominant disease characterized by elevated levels of low-density lipoprotein-cholesterol (LDL-C). Phenotypic expression is highly variable, being influenced by diet, age, gender, body mass index, apolipoprotein E genotype and type of LDL-receptor gene mutation. Microsomal triglyceride (TG) transfer protein (MTP) is a protein involved in lipid metabolism. Polymorphism MTP -493 GT has been shown to modulate lipid levels in several populations. To analyse the effect of this polymorphism in the lipid phenotype expression of FH and treatment response, we studied a sample of 222 Spanish FH patients, of whom 147 were studied before and after treatment with 20 mg of atorvastatin daily during 6 weeks. The variant was analysed by polymerase chain reaction amplification and single-strand confirmation polymorphism. Treatment reduced LDL-C, total cholesterol and TGs. Baseline fasting TGs and very-low-density lipoprotein cholesterol levels were lower in female T allele carriers (TG: 111±51 mg/dl GG, 89±35 mg/dl GT, 83±26 mg/dl TT, P=0.022; very-low-density lipoprotein cholesterol: 24±13 mg/dl GG, 16±5 mg/dl GT, 17±5 mg/dl TT, P=0.018). Triglyceride response to atorvastatin was modulated by this polymorphism in men (P=0.009), but not in women, although differences between genotypes were maintained after treatment. In conclusion, the MTP -493 GT polymorphism modulates pre- and post-treatment plasma TG values of FH in Spanish subjects in a gender-specific way. Other environmental and genetic factors likely also modulate this response. [ABSTRACT FROM AUTHOR]