Materials and methods. An ~1.75-kb promoter region of SERCA2 gene was cloned with the pGL3 luciferase vector. The direct effects of Ang II on SERCA2 gene expression in HL-1 atrial myocytes were examined by promoter activity assay, followed by Western blot analysis for protein levels and quantitative real-time reverse transcription polymerase chain reaction for mRNA amounts.

Results. Ang II did not increase the promoter activity of the 1,754-bp promoter-receptor construct of the SERCA2 gene. The levels of SERCA2 protein and mRNA were also unchanged at different time points after Ang II treatment.

Conclusions. Although Ang II had prominent effects on SERCA2 in ventricular myocytes, it did not alter SERCA2 gene expression and protein levels in atrial myocytes. We provide a model for further investigation of the regulation of SERCA2 gene expression in atrial myocytes.

Methods. Infusion of subpressor doses of aldosterone with subcutaneously implanted mini-osmotic pumps (0.05 mg/kg/day) to rats for 21 days induced the development of endothelial dysfunction. In order to evaluate endothelial function, isometric tension studies were performed in response to acetylcholine and sodium nitroprusside.Additionally, PAR (the end product of activated PARP) and PARP-1 expressions in the endothelium of thoracic aortas were evaluated by immunohistochemistry.

Results. There was a significant loss of endothelium-dependent vasodilatation in response to acetylcholine in aldosterone-infused rats. In animals treated with 1,5-isoquinolinediol, the effect of aldosterone on vascular responsiveness was less than the untreated groups. Immunohistochemical studies demonstrated that aldosterone administration increased PAR and PARP-1 expressions in the endothelium of thoracic aortas, whereas PARP inhibition decreased their expressions to control levels.

Conclusion. Our results indicate that PARP activation in the vascular system may be a contributory factor to the impaired endothelial function associated with aldosterone administration.

Materials and methods. Chronically prepared near-term ovine foetuses (control and experimental: n=5, each group) were used.After 4—5 days’ surgical recovery, conscious ewes and their foetuses were tested in vivo.

Results. In response to intravenous atropine, foetal systolic, diastolic, and mean arterial pressure, as well as heart rate, increased immediately. Inhibition of muscarinic systems in the circulation caused a reduction of plasma angiotensin II levels, while angiotensin I in the circulation remained unchanged in the foetus. In addition, foetal plasma aldosterone levels were significantly increased following blockade of the cholinergic receptor, while other hormones, including arginine vasopressin, adrenocorticotrophic hormone, and atrial natriuretic peptide, were not changed in foetal blood under the same condition.

Conclusions. The results suggest that foetal automatic systems, not those hormonal factors tested, play a major role in cholinergic mechanisms mediating cardiovascular control. Furthermore, the data provide new information on how muscarinic inhibition affects renin-angiotensin system and adrenal cortex functions. Key words: aldosterone, angiotensin-converting enzyme, autonomic regulation, foetus

Methods. After placebo run-in, 842 patients (mean sitting diastolic blood pressure (BP) 95—109 mmHg) were randomised to aliskiren 150 mg or ramipril 5 mg. Dose titration and hydrochlorothiazide addition were allowed after Week 6 and 12, respectively, for inadequate BP control. Patients completing active treatment were re-randomised to current regimen or placebo during a 4-week posttreatment phase.

Results. BP reductions were independent of baseline PRA at Week 12, were greater with aliskiren- than ramipril-based therapy at Week 26 (17.9/13.3 vs. 15.2/12.0 mmHg, p<0.05) and persisted for longer after stopping aliskiren. Aliskiren-based therapy reduced geometric mean PRA (–63%, p<0.05; n=103), while ramipril-based therapy increased PRA (+143%, p<0.05; n=100) at Week 26; PRC increased in both groups (aliskiren: +224% [n=33], ramipril: +145% [n=39], both p<0.05). Four weeks after stopping aliskiren-based therapy, PRA remained 52% below pre-treatment baseline; PRA returned to baseline 2 weeks after stopping ramipril-based therapy.

Conclusions. Aliskiren-based therapy produced sustained BP and PRA reductions over 26 weeks; ramipril-based therapy lowered BP and increased PRA. PRA reductions persisted 4 weeks after stopping aliskiren, suggesting an inhibitory effect beyond the elimination half-life of the drug.

Methods. The patients were treated for a 12-month period with a candesartan-based regimen (8/16 mg + hydrochlorothiazide12.5 mg + additional drugs to target blood pressure < 140/90 mmHg [< 130/80 in diabetics]). Cornell voltage index (CorV), Cornell product (CorP), Sokolow-Lyon voltage index (SokV), and Sokolow-Lyon product (SokP) were calculated. In total 276 patients were included, 51 with diabetes.

Results. At study end, blood pressure was reduced 19.0±9.2/7.3±3.4 mmHg in diabetic patients and 18.8±9.1/8.0±3.2 mmHg in non-diabetic subjects (both p<0.01 vs. baseline; p=0.85 between groups).At baseline, 37.5% of diabetic and 26.4% of non-diabetic patients fulfilled criteria of ECG-LVH by CorP (p=0.02), 25.7% and 23.2%, respectively, by SokP (p=0.18), 11.8% and 13.7% by CorV (p=0.16), and 14.3% and 11.6% by SokV (p=0.10).At study end, the prevalence of ECG-LVH was reduced to 25.1% (relative risk reduction [RRR] 33.3%, p=0.001) and 18.2% (RRR 29.2%, p=0.001) by CorP and SokP, in diabetic patients, respectively. In non-diabetic patients, only the CorP criterion showed a significant decrease (RRR 18.9%, p=0.01). No significant changes were observed by other criteria.The RRR of ECG-LVH with treatment was significantly higher in diabetics according to CorP and SokP criteria.

Conclusions. The prevalence of ECG-LVH detected by CorP was higher in diabetics. Diabetics achieved higher reductions in ECG-LVH prevalence than non-diabetics with a candesartan-based regimen.

Subjects and methods. The present study included a total number of 221 subjects (107 myocardial infarction patients and 114 age- and sex-matched controls). Demographic and clinical characteristics were collected. Lipid profiles were estimated. DNA was isolated and the angiotensin II type 1 receptor gene A/C polymorphism was determined by polymerase chain reaction.

Results. Comparison of the lipid profiles between patients and controls showed that patients had statistically highly significant values (p=0.0001).The CC genotype of the angiotensin II type 1 receptor was not associated with myocardial infarction patients when compared to controls. CC vs. AA was ² = 2.08, odds ratio 2.30, 95% confidence interval 0.72 — 7.23, and p value was 0.14.

Conclusion. The angiotensin II type 1 receptor CC genotype is not a risk factor for myocardial infarction in patients in a South Indian population.

Subjects and methods. In the present case-control study, genotyping of 187 unrelated patients with MDD (44.89±12.92 years) and 207 unrelated healthy controls (41.34±9.76 years) from the northeastern part of Thailand was performed using polymerase chain reaction-restriction fragment length polymorphism technique.

Results. Comparing the two groups, no significant difference was observed with regard to either genotype distributions or allele frequencies of the –93T/C SNP of ACE. For the –240A/T SNP, a significant difference in genotype distributions was found (²=6.65, df=2, p=0.036).The presence of the –240A allele of ACE was associated with a decreased risk for MDD compared with the –240T allele (²=4.24, df=1, p=0.040, odds ratio=0.702 [95% confidence interval=0.508—0.971]). Moreover, haplotype frequency analysis revealed that the –240T/—93T combination was significantly over-represented in patients with MDD in comparison with controls (13.6% and 6.8%, p=0.002 on ² test, empirical p=0.004).

Conclusions. In the present investigation, an association between the –240A allele and a reduced risk for MDD was observed, but the genotype distributions of controls were only just in marginal agreement with Hardy-Weinberg equilibrium.The T-T haplotype in the ACE gene was significantly associated with an increased risk for MDD.