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Diabetes has been related to changes in vascular responses, mainly an increase in the vasoconstrictor responses and a decrease in the vasodilator responses. The literature has now begun to study the effects of diabetes in the early stages of development; the first studies on these stages indicate that diabetes produces different changes compared to the advanced stages. For that reason, the aim of this work was to evaluate the responses to norepinephrine and dopamine on normotensive and hypertensive rats with 4 weeks of diabetes evolution. The results showed that 4 weeks of diabetes produces a decrease of the vasopressor response to both agents (norepinephrine and dopamine). These results suggest that in the early stages, there are changes that help to decrease the pressor responses and these changes could disappear in the advanced stages. [ABSTRACT FROM AUTHOR]

Background. Diabetic nephropathy (DN) is a severe long-term complication of diabetes characterized by continuous albuminuria, a relentless decline in renal function, and an increased arterial blood pressure. Aims. Our aim was to find out if single nucleotide polymorphisms (SNPs) within the SLC22A1, SLC22A2, and SLC22A3 genes encoding organic cation transporters (OCTs) associate with DN or hypertension. Subjects and methods. We selected 90 SNPs (≈1 SNP/4 kb) in and surrounding SLC22A1, SLC22A2, and SLC22A3 using the HapMap data. The SNPs were tested for association with DN and hypertension in 1,086 unrelated Finnish patients with type 1 diabetes mellitus (T1DM). Eight of the SNPs were genotyped in 1,252 additional Finnish patients to verify the findings. Results. We detected nominal evidence of association ( P < 0.05) between the SLC22A2 (SNPs rs653753, rs596881, and rs316019) and SLC22A3 (SNPs rs376563, rs2048327, rs2457576, and rs1567438) genes and DN and hypertension in Finnish men with T1DM. We were not, however, able to replicate the associations, and none of them reached the significance limit adjusted for multiple testing ( P < 0.00009). Conclusions. There was no clear association between the SLC22A1, SLC22A2, and SLC22A3 genes and DN or hypertension. Although several SLC22A2 and SLC22A3 SNPs indicated association, lack of association was evident after the replication study. [ABSTRACT FROM AUTHOR]

Endothelial dysfunction plays an important role in the pathogenesis of hypertension. Other risk factors of atherosclerosis also affect its development. The aim of the study was to assess nitric oxide metabolites concentration (nitrites and nitrates Nox) and endothelin (ET-1) in plasma and cyclic 3,5-guanosine monophosphate (cGMP) in 24 h-urine collection in patients with noncomplicated hypertension without risk factors of atherosclerosis and in hypertensive patients with coronary artery disease (CAD). Sixty-eight subjects were included in the study (44 men, 24 women), aged 47 ± 76 years, allotted into four groups: I - controls (18 clinically healthy subjects); II - 12 subjects with hypertension without risk factors of atherosclerosis; III - 16 subjects with hypertension and risk factors of atherosclerosis; and IV - 22 subjects with hypertension and CAD. Plasma NOx concentration was determined using the Greiss method, plasma ET-1 by ELISA, and urine cGMP using the immunoenzymatic method. Plasma NOx concentration was 14.00 ± 6.88 μmol/L in group I, in group II - 18.62 ± 5.84 μmol, in group III - 9.96 ± 4.72 μmol/L, and in group IV - 8.78 ± 3.72 μmol/L. Statistically significant differences were between groups I and III (p < 0.05) and I and IV (p < 0.04) and groups II and III (p < 0.01) and II and IV (p < 0.01). The concentration of cGMP in 24 h urine collection was in group I - 40 ± 24 pmol/L; in group II - 54 ± 41 pmol/L; in group III - 38 ± 32 pmol/L; and in group IV - 42 ± 36 pmol/L. There were no significant differences between the groups. Plasma ET-1 concentration was 3.86 ± 0.52 pg/mL in group I, in group II - 4.05 ± 0.71 pg/mL, in group III - 4.22 ± 0.79 pg/mL and in group IV - 4.38 ± 0.75 pg/mL. Statistically significant differences were between group I and III (p < 0.05), I and IV (p < 0.03), and between group II and IV (p < 0.04). Endothelial dysfunction was not found in hypertensive patients without a family history of cardiovascular diseases and without other risk factors of atherosclerosis. Deterioration of endothelial function was observed in patients with hypertension with risk factors of atherosclerosis. It was most pronounced in those with CAD. [ABSTRACT FROM AUTHOR]

Rheumatoid arthritis (RA) associates with excess cardiovascular (CV) morbidity and mortality. Hypertension, a highly prevalent entity in RA, has been associated with the endothelin-1 (ET-1) gene locus (EDN1) in some groups, such as Afro-Caribbean, the obese, and in low-renin states, but not in the general population as a whole. High levels of plasma ET-1 have been observed in RA. This study evaluated the potential association of EDN1 gene locus and serum ET-1 levels with hypertension in patients with RA. Genomic DNA and serum samples were collected from 397 well-characterized RA patients; DNA was also available from 401 local general population controls without RA. To explore the overall relevance of EDN1, two suitable single-nucleotide polymorphisms (SNPs), rs1800541 and rs5370, were selected and haplotype analysis was performed. Both SNPs were identified using real-time polymerase chain reaction (PCR) and melting curve analysis. Genetic analysis was related to hypertension as dichotomous trait and to blood pressure indices as continuous variables. Serum endothelin levels were also assessed in the RA patients. No genotype or haplotype differences were observed between RA and control subjects. Within RA, logistic regression analysis of each SNP separately revealed a threefold increase in the adjusted odds of being hypertensive of rs5370 TT homozygotes compared to GG homozygotes (OR = 2.89, 95%CI: 1.02 to 8.19). After adjustment for multiple potential confounders, haplotype analysis revealed an additive effect of the rs1800541-rs5370 T-T haplotype on hypertension (OR = 2.96, 95%CI: 1.28 to 6.86; p = .011), systolic blood pressure (SBP) (β = 6.75 ± 2.57 mm Hg; p = .009), and pulse pressure (PP) (β = 4.37 ± 2.12 mm Hg; p = .040). There was an increased prevalence of raised ET-1 levels amongst hypertensive RA patients, whereas a similar trend was observed for T-T haplotype carriers. RA patients who carry the rs1800541-rs5370 T-T EDN1 haplotype appear more likely to be hypertensive with an increased SBP and PP. These findings, if replicated in future studies, could be used as a screening tool for RA patients at increased hypertension, and thus cardiovascular, risk. [ABSTRACT FROM AUTHOR]

Hypertension and obesity are risk factors for coronary heart diseases in adults. In turn, childhood overweight and high blood pressure increase the risk of subsequent obesity and hypertension in adulthood. Human obesity is characterized by profound alterations of hemodynamic and metabolic states. Whether these alterations involve sympathetic nervous system control on cardiac function is controversial. We report the results of our study, conducted in a sample of obese adolescents by using power spectral analysis of heart rate variability. An increase in sympathetic tone coupled with a reduction in vagal tone was found. This allowed us to hypothesize that autonomic nervous system changes depend on the time course of obesity development. It is still unclear if treatment of obesity in adolescence prevents subsequent autonomic imbalance and hypertension. [ABSTRACT FROM AUTHOR]