Abstract-Detection of hypertension and blood pressure control are critically important for reducing the risk of heart attacks and strokes. We analyzed the trends in the prevalence, awareness, treatment,

OBJECTIVE -We investigated the association of the metabolic syndrome with new-onset diabetes in the Hong Kong Cardiovascular Risk Factor Prevalence Study cohort.RESEARCH DESIGN AND METHODS -We followed up on 1,679 subjects without diabetes at baseline. Those with a previous diagnosis of diabetes or those who were receiving drug treatment were considered to be diabetic. The remaining subjects underwent a 75-g oral glucose tolerance test (OGTT). Diabetes was defined by plasma glucose Ն7.0 mmol/l with fasting and/or Ն11.1 mmol/l at 2 h.RESULTS -The prevalences of the metabolic syndrome at baseline were 14.5 and 11.4%, respectively, according to U.S. National Cholesterol Education Program (NCEP) and International Diabetes Federation (IDF) criteria. After a median of 6.4 years, there were 66 and 54 new cases of diabetes in men and women, respectively. The metabolic syndrome at baseline predicted incident diabetes. Hazard ratios (HRs) for the NCEP and IDF definitions of the syndrome were 4.1 [95% CI 2.8 -6.0] and 3.5 [2.3-5.2], respectively. HRs for fasting plasma glucose (FPG) Ն6.1 or 5.6 mmol/l were 6.9 [4.1-11.5] and 4.1 [2.8 -6.0], respectively. The NCEP and IDF criteria had 41.9 and 31.7% sensitivity and 87.5 and 90.2% specificity, respectively. Their positive predictive values were low, ϳ20%, but their negative predictive values were ϳ95%.CONCLUSIONS -The metabolic syndrome, particularly its component, elevated FPG, predicts diabetes in Chinese. An individual without the metabolic syndrome is unlikely to develop diabetes, but one who has it should practice therapeutic lifestyle changes and have periodic FPG measurements to detect new-onset diabetes. Diabetes Care 30:1430-1436, 2007T he metabolic syndrome has been promoted as a clinical tool for identifying individuals predisposed to diabetes and/or adverse cardiovascular outcomes (1-7). Attempts have been made by different consensus groups to produce diagnostic criteria for the syndrome, but there is still some controversy. The pathogenetic mechanism underlying the metabolic syndrome remains uncertain, although central obesity and insulin resistance have been proposed to play a causative role. Because insulin resistance, together with hyperinsulinemia, is a fundamental metabolic abnormality in type 2 diabetes, the metabolic syndrome may be expected to be a good predictor of the development of the latter. Asians are thought to have a higher body fat percentage and cardiovascular risks than Caucasians at a given BMI (8). These factors raise concerns that definitions of the metabolic syndrome for Caucasians, when applied to Asian populations, would underestimate the population at risk of developing adverse outcomes such as type 2 diabetes, cardiovascular disease, and mortality. Therefore, validation of the predictive value of the metabolic syndrome needs to be established in population-based cohorts of different ethnicities. The International Diabetes Federation (IDF) proposed a new definition of the metabolic syndrome, which uses ethnicspecific central obesity cri...

Plasma urotensin II was raised in hypertensive patients compared to normotensive controls, and was directly related to systolic blood pressure. Our findings raise the possibility that urotensin II may have an aetiological role in hypertension and its complications.

The prevalence, awareness, treatment, and control of hypertension in the United States are analyzed using the National Health and Nutrition Examination Survey (NHANES) database covering the period 1988–2002. Mean body mass index was 26.1±0.1 kg/m2 in 1988–1991 and 27.9±0.2 kg/m2 in 2001–2002 (p<0.001). In the same period, the prevalence of diabetes mellitus increased from 5.0% to 6.5% (p=0.03). Diastolic blood pressure was 73.3±0.2 mm Hg in 1988–1991 and 71.6±0.4 mm Hg in 2001–2002 (p<0.001). Among the 18–39 years and 60 years and older age groups, the prevalence of hypertension increased significantly since 1988–1991. Multiple regression shows age, body mass index, and being non‐Hispanic black were significantly associated with hypertension. In the period 1988–2002, the percentage receiving treatment and the percentage with blood pressure controlled increased significantly. In 2001–2002, significantly more people with hypertension and diabetes reached a blood pressure target of <130/85 mm Hg. Overall, the control rates were low, especially among middle‐aged Mexican‐American men (8%).

BACkgROuNdThe metabolic syndrome is a predictor of diabetes and coronary events. We hypothesized that it also predicts hypertension.METhOdS a total of 1,944 subjects (901 men and 1,043 women; age 46 ± 12 years) from the Hong Kong Cardiovascular Risk Factor Prevalence Survey were recruited in 1995-1996 and restudied in 2000-2004. The prevalence of hypertension and factors predicting its development were determined. RESulTSIn 2000-2004, hypertension was found in 23.2% of the men and 17.2% of the women. Of the 1,602 subjects who were normotensive at baseline, 258 subjects developed hypertension after a median interval of 6.4 years. according to the National Cholesterol Education Program (NCEP) and International Diabetes Federation (IDF) criteria, the hazard ratios associated with the metabolic syndrome were 1.89 (95% confidence interval (CI): 1.41-2.54) and 1.72 (95% CI: 1.24-2.39), respectively. The positive and negative predictive values of the metabolic syndrome for identifying subjects who will develop hypertension in this population were 34.7 and 85.4% (NCEP criteria), and 33.1 and 85.5% (IDF criteria), respectively. The development of hypertension was related to the number of components of the metabolic syndrome (other than raised blood pressure), present in men (P = 0.003) and in women (P = 0.001). Using multivariate analysis, age, baseline systolic blood pressure (SBP), body mass index (BMI), and the triglycerides/high-density lipoprotein (HDL) ratio were found to be significant predictors of the development of hypertension. Compared with optimal blood pressure, the hazards of developing hypertension associated with normal or high-normal blood pressure were 2.31 (95% CI: 1.68-3.17) and 3.48 (95% CI: 2.52-4.81), respectively. CONCluSiONSBlood pressure, when not optimal, is the predominant predictor of hypertension. The metabolic syndrome contributes to the risk, especially when blood pressure is optimal.

The authors studied the prevalence of the metabolic syndrome in the 1999-2002 National Health and Nutrition Examination Survey (NHANES) according to the World Health Organization, National Cholesterol Education Program (NCEP), and International Diabetes Federation (IDF) definitions. There was 92.9% agreement between the NCEP and IDF definitions. The IDF prevalence was higher (p = 0.001) due to more men fulfilling its criteria than the NCEP's (39.9 +/- 1.7% vs. 33.6 +/- 1.6%; p = 0.007). If central obesity were not a prerequisite, the IDF prevalence would increase slightly to 40.3 +/- 1.1%. Subjects categorized as having the metabolic syndrome under IDF but not NCEP tended to be men, younger, and leaner. Their prevalence of self-reported coronary heart disease was not significantly different from that of other metabolic syndrome patients. Whether waist circumference is a prerequisite does not affect the diagnosis of the metabolic syndrome in the United States. The IDF definition identifies additional individuals at risk for cardiovascular disease.

We studied single nucleotide polymorphisms (SNPs) and haplotypes in the urotensin-II (UTS2) and urotensin-II receptor gene (UTS2R) in Hong Kong Chinese (224 hypertensive and 306 normotensive unrelated subjects) and their relation to hypertension and the metabolic syndrome. For UTS2, the GGT haplotype (-605G, 143G and 3836T) was associated with higher plasma level of U-II and insulin, and higher homeostasis model assessment of insulin resistance index and beta-cell function. For UTS2R, the AC haplotype (-11640A and -8515C) was associated with higher 2 h plasma glucose after a 75 g oral glucose load. Therefore, U-II and its receptor may play a role in insulin resistance.

Objectives-Adenosine is a cAMP-elevating vasodilator that induces both endothelium-dependent and -independentvasorelaxation. An increase in cytosolic Ca 2ϩ ([Ca 2ϩ ] i ) is a crucial early signal in the endothelium-dependent relaxation elicited by adenosine. This study explored the molecular identity of channels that mediate adenosine-induced Ca 2ϩ influx in vascular endothelial cells. Methods and Results-Adenosine-induced Ca 2ϩ influx was markedly reduced by L-cis-diltiazem and LY-83583, two selective inhibitors for cyclic nucleotide-gated (CNG) channels, in H5V endothelial cells and primary cultured bovine aortic endothelial cells (BAECs). The Ca 2ϩ influx was also inhibited by 2 adenylyl cyclase inhibitors MDL-12330A and SQ-22536, and by 2 A 2B receptor inhibitors MRS-1754 and 8-SPT, but not by an A 2A receptor inhibitor SCH-58261 or a guanylyl cyclase inhibitor ODQ. Patch clamp experiments recorded an adenosine-induced current that could be inhibited by L-cis-diltiazem and LY-83583. A CNGA2-specific siRNA markedly decreased the Ca 2ϩ influx and the cation current in H5V cells. Furthermore, L-cis-diltiazem inhibited the endothelial Ca 2ϩ influx in mouse aortic strips, and it also reduced 5-N-ethylcarboxamidoadenosine (NECA, an A 2 adenosine receptor agonist)-induced vasorelaxation. Conclusion-CNGA2 channels play a key role in adenosine-induced endothelial Ca 2ϩ influx and vasorelaxation. It is likely that adenosine acts through A 2B receptors and adenylyl cyclases to stimulate CNGA2. A denosine is an endogenous nucleoside with potent vasodilatory capacities in many vascular beds. 1 Adenosine can be released from myocardium, endothelial cells, and skeletal muscles as a result of metabolism. The released adenosine then elicits vasorelaxation either by directly stimulating A 2 -adenosine receptors in vascular smooth muscle cells, causing subsequent vasorelaxation, 1 or by indirectly acting on vascular endothelial cells, triggering endotheliumdependent vasorelaxation. [1][2][3] Adenosine induces the endothelium-dependent vasorelaxation either via a Ca 2ϩ -dependent mechanism 3-5 or a Ca 2ϩ -independent mechanism. 2 In the former case, the adenosineinduced [Ca 2ϩ ] i rise stimulates endothelial cells to release vasorelaxants such as nitric oxide (NO) 3,6 and endotheliumderived hyperpolarizing factor (EDHF). 7 These vasodilators diffuse to nearby smooth muscle cells, causing vascular smooth muscle relaxation. At least in some arteries, this [Ca 2ϩ ] i rise is a prerequisite for adenosine-induced vasodilator release and vasorelaxation. [3][4][5] For example, in skeletal muscle arterioles, adenosine elicits an endothelial [Ca 2ϩ ] i rise, 3,5 and chelation of endothelial [Ca 2ϩ ] i with intraluminal perfusion of BAPTA-AM abolishes the adenosine-induced vasorelaxation, indicating an obligatory role of endothelial [Ca 2ϩ ] i in this relaxation. 3,5 In another study, it was found that adenosine induces NO release from rat aortic endothelium in situ, and this NO release requires Ca 2ϩ influx. 4...