Dementia Rating Scale-2 normative data for middle-and older-aged Castilian speaking Spaniards.

OBJECTIVES: The Dementia Rating Scale-2 (DRS-2) is frequently used as a dementia screening tool in clinical and research settings in Spain. The present study describes DRS-2 Total and subscale scores in community-dwelling Spaniards, aged 50-71, and provides normative data for its use in Castilian Spanish-speaking individuals. METHODS: The sample consisted of 798 individuals who participated in an observational study on essential hypertension. Mean age was 62.8 years (SD = 5.4), mean education was 8.6 years (SD = 3.4) with 47.9% females. Almost all of them were receiving blood pressure-lowering drugs (93%) and most of them had fairly well-managed blood pressure control (M systolic/diastolic blood pressure = 142.3/77.0 ± 16.0/9.2 mm Hg). We applied a previously described method of data normalization from the Mayo's Older Americans Normative Studies to obtain the Castilian Spanish DRS-2 norms. RESULTS: Worse performance on Total and subscale scores was associated with older age (p < .05) and fewer years of education (p < .001). Women obtained lower raw Total scores than men (131.68 ± 7.2 vs. 133.10 ± 6.90, p < .005), but had fewer years of education (7.96 ± 3.33 vs. 9.17 ± 3.45, p < .001). This gender difference disappeared after correcting for age and years of education. Total and subscale scores are presented adjusted by age, and normative data are shown for Total scores adjusted by age and years of education. CONCLUSIONS: These norms are useful for studying cognitive status and cognitive decline in research and clinical settings in Castilian Spanish-speaking populations.

Angiotensin-converting enzyme i/d polymorphism in patients with malignant hypertension.

The angiotensin-converting enzyme (ACE) gene has been implicated in the manifestation of the phenotype of malignant hypertension (MH). In 1990 the ACE gene polymorphism characterized by the insertion or deletion of a 287-base pair fragment in the 17q23 chromosome was identified. The DD genotype is associated with increased tissue and circulating ACE levels and elevated angiotensin II. ACE polymorphism was studied in 48 patients with MH, 25 patients with non-MH, and a control group of 78 normotensive individuals by real-time polymerase chain reaction using the LightCycler system (Roche Diagnostics Corporation, Indianapolis, IN). The DD genotype was found statistically more frequently in MH patients than controls (p=0.028; odds ratio, 2.5; confidence interval, 1.1-5.5). Presence of the DD genotype of the ACE gene is more frequent in MH patients than in controls, indicating that this genotype could be a significant risk factor and a predictor for the development of MH.

Sex steroid regulation and identification of different transcription units of the SA gene in mouse kidney.

Although the SA gene was first identified as a putative candidate gene to understand the molecular basis of hypertension in rat and humans, the concept has not been supported in recently generated SA-null mice. We had first identified the mouse SA gene on the basis of its strong androgenic regulation in mouse kidney and further characterized its genomic organization, transcription start site and chromosomal location. Northern blot, RT-PCR and in situ hybridization assays determined mouse strain, tissue distribution, sex-hormone dependence and cell expression of the SA) mRNA. Kidney and liver constitute the main expression sites of the SA gene; in particular it is expressed in epithelial proximal tubule cells in the presence of androgens. This androgen-dependent expression is abrogated when estrogens are also present. By using the sensitive RT-PCR technique, minor SA expression sites, corresponding to testes, stomach, heart and lung, have also appeared. Like in kidney, expression of the SA gene in heart and lung is androgen-dependent. Production of rabbit antibodies against SA-synthetic peptides identified the SA protein, a moiety of unknown function, which has been defined as a member of the acyl-CoA synthetase family. We have determined that the SA protein follows the same distribution and regulation as its corresponding mRNA. Transient transfection assays followed by confocal microscopy identified the mitochondria of proximal tubule-derived PCT3 cells as the subcellular location of the SA protein. Different transcriptional units produced by splicing events, occurring before the translation initiation site, have been identified from mouse kidney. This work provides the basis to further understand the molecular mechanisms that control the sex-steroid-dependent expression of the SA gene in mouse kidney, heart and lung, where SA is also expressed in an androgen-dependent manner.

A randomized controlled study of CPAP effect on plasma aldosterone concentration in patients with resistant hypertension and obstructive sleep apnea.

OBJECTIVE: The high prevalence of obstructive sleep apnea in patients with resistant hypertension could be mediated by an activation of the renin-angiotensin-aldosterone system. This study assessed the impact of continuous positive airway pressure (CPAP) treatment on plasma aldosterone concentration (PAC). METHODS: One hundred and twenty-four patients with resistant hypertension were assessed, and those who fulfilled inclusion criteria (n = 116) underwent full night polysomnography, 24-h ambulatory blood pressure monitoring, and PAC measurement. Patients with an apnea-hypopnea index above 15 (n = 102) were randomized to CPAP (n = 50) or to conventional treatment (n = 52) for 3 months. RESULTS: Seventy-eight patients completed the follow-up (36 CPAP, 42 conventional treatment); 58 had true resistant hypertension (74.3%), whereas 20 had white-coat resistant hypertension (25.6%). Most patients were men (70.7%), age 58.3 ±â€Š9.4 years, and the mean apnea-hypopnea index was 50.1 ±â€Š21.6. In patients with true resistant hypertension, CPAP achieved a significant decrease in most 24-h BP measurements and a nonsignificant decrease in PAC (25 ±â€Š8.7 vs. 22.7 ±â€Š9 ng/dl; P < 0.182). In patients with white-coat resistant hypertension, CPAP achieved a significant decrease in PAC (26.1 ±â€Š11.2 vs. 18.9 ±â€Š10.1 ng/dl; P < 0.041) and in night-time DBP. After adjustment, a weak but significant association was found between cumulative time spent with SaO2 below 90% (CT90%) and baseline PAC (P < 0.047, R 0.019), and between changes in PAC and changes in office DBP (P < 0.020, R 0.083) CONCLUSIONS:: Night-time hypoxemia and changes in DBP showed an association with baseline and changes in PAC, respectively. CPAP achieved a significant reduction in PAC only in patients with white-coat resistant hypertension, although the CPAP effect on BP was highest in patients with true resistant hypertension.

Continuous positive airway pressure treatment in sleep apnea patients with resistant hypertension: a randomized, controlled trial.

OBJECTIVES: This controlled trial assessed the effect of continuous positive airway pressure (CPAP) on blood pressure (BP) in patients with obstructive sleep apnea (OSA) and resistant hypertension (RH). METHODS: We evaluated 96 patients with resistant hypertension, defined as clinic BP at least 140/90 mmHg despite treatment with at least three drugs at adequate doses, including a diuretic. Patients underwent a polysomnography and a 24-h ambulatory BP monitoring (ABPM). They were classified as consulting room or ABPM-confirmed resistant hypertension, according to 24-h BP lower or higher than 125/80 mmHg. Patients with an apnea-hypopnea index at least 15 events/h (n = 75) were randomized to receive either CPAP added to conventional treatment (n = 38) or conventional medical treatment alone (n = 37). ABPM was repeated at 3 months. The main outcome was the change in systolic and diastolic BP. RESULTS: Sixty-four patients completed the follow-up. Patients with ABPM-confirmed resistant hypertension treated with CPAP (n = 20), unlike those treated with conventional treatment (n = 21), showed a decrease in 24-h diastolic BP (-4.9 ± 6.4 vs. 0.1 ± 7.3 mmHg, P = 0.027). Patients who used CPAP > 5.8 h showed a greater reduction in daytime diastolic BP {-6.12 mmHg [confidence interval (CI) -1.45; -10.82], P = 0.004}, 24-h diastolic BP (-6.98 mmHg [CI -1.86; -12.1], P = 0.009) and 24-h systolic BP (-9.71 mmHg [CI -0.20; -19.22], P = 0.046). The number of patients with a dipping pattern significantly increased in the CPAP group (51.7% vs. 24.1%, P = 0.008). CONCLUSION: In patients with resistant hypertension and OSA, CPAP treatment for 3 months achieves reductions in 24-h BP. This effect is seen in patients with ABPM-confirmed resistant hypertension who use CPAP more than 5.8 h.