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The purpose of this study was to explore whether dysglycemia, and/or an increased body mass index, and/or an increased waist/hip ratio increased the risk of hypertension in a lean population of South China. The association among dysglycemia, obesity, and hypertension has been well documented in Western populations. A stratified cluster sampling method was used according to the National Diabetes Mellitus Epidemiology Survey Program in 1998. Blood pressure, fasting plasma glucose, and plasma glucose were measured 2 hours after 75-g oral glucose consumption using the enzymatic method in the morning. Body height, weight, and waist and hip measurements were also collected for the survey. The criteria for the diagnosis of hypertension and diabetes mellitus, including impaired glucose tolerance (IGT), were those published by the World Health Organization in 1999. A total of 11,402 participants were included in the investigation (5,195 men and 6,207 women; age 20 to 74 years). A total of 1,775 cases of hypertension were confirmed in the survey. The prevalence of hypertension was significantly higher in those with diabetes mellitus than in those with a normal blood glucose level, in those with IGT than in those with normal glucose tolerance test findings, and in obese participants than in those with a normal weight (45.5% vs 14.4%, 32.2% vs 14.5%, and 20.6% vs 12.1%, respectively). Multiple logistic regression analysis indicated that age and gender-adjusted odds ratio of hypertension was 2.24 (95% confidence interval 1.88 to 2.68) with IGT compared with those without IGT. The odds ratio for hypertension associated with an increased body mass index and waist/hip ratio was 1.19 (95% confidence interval 1.17 to 1.21) and 1.08 (95% confidence interval 1.07 to 1.09), respectively. In conclusion, the data from an epidemiologic study in South China demonstrated that dysglycemia and increased body mass index and/or waist/hip ratio increase the risk of hypertension even in a lean Chinese population. [Copyright &y& Elsevier]

Abstract: Aim of this study: The panax notoginseng saponins (PNS) have been clinically used for the treatment of cardiovascular diseases and stroke in China. Evidences demonstrated that PNS could protect cardiomyocytes from injury induced by ischemia, but the underlying molecular mechanisms of this protective effect are still unclear. This study was aimed to investigate the protective effect and potential molecular mechanisms of PNS on apoptosis in H9c2 cells in vitro and rat myocardial ischemia injury model in vivo. Materials and methods: H9c2 cells subjected to serum, glucose and oxygen deprivation (SGOD) were used as in vitro models and SD rats subjected to left anterior descending (LAD) coronary artery ligation were used as in vivo models. The anti-apoptotic effect of PNS was evaluated by Annexin V/PI analysis or TUNEL assay. Mitochondrial membrane potential (Δψm) was detected by JC-1 analysis. The expression of Akt and phosphorylated Akt (p-Akt) were detected by western blot assay. Results: PNS exhibited anti-apoptotic effect both in H9c2 cells and in ischemic myocardial tissues. However, the effect was blocked in vitro by LY294002, a specific PI3K inhibitor. The anti-apoptotic effect of PNS was mediated by stabilizing Δψm in H9c2 cells. Furthermore the indices of the left ventricular ejection fractions (EF), left ventricular fractional shortening (FS), left ventricular dimensions at end diastole (LVDd) and left ventricular dimensions at end systole (LVDs) suggested that PNS improved rats cardiac function. PNS significantly increased p-Akt both in H9c2 cells and in ischemic myocardial tissues and this effect was also blocked by LY294002 in H9c2 cells. Conclusion: Results of this study suggested that PNS could protect myocardial cells from apoptosis induced by ischemia in both the in vitro and in vivo models through activating PI3K/Akt signaling pathway. [Copyright &y& Elsevier]

Abstract: Carvedilol is a β- and α1-adrenoceptor antagonist. It is widely used in the treatment of cardiovascular diseases including atrial arrhythmias. However, it is unclear whether carvedilol may affect the repolarization currents, transient outward K+ current (I to) and ultra-rapid delayed rectifier K+ current (I Kur) in the human atrium. The present study evaluated effects of carvedilol on I to and I Kur in isolated human atrial myocytes by whole-cell patch-clamp recording technique. We found that carvedilol reversibly inhibited I to and I Kur in a concentration-dependent manner. Carvedilol (0.3 μM) suppressed I to from 9.2±0.5 pA/pF to 4.8±0.5 pA/pF (P <0.01) and I Kur from 3.6±0.5 pA/pF to 1.9±0.3 pA/pF (P <0.01) at +50 mV. I to was inhibited in a voltage-dependent manner, being significantly attenuated at test potentials from +10 to +50 mV, whereas the inhibition of I Kur was independent. The concentration giving a 50% inhibition was 0.50 μM for I to and 0.39 μM for I Kur. Voltage-dependence of activation, inactivation and time-dependent recovery from inactivation of I to were not altered by carvedilol. However, time to peak and time-dependent inactivation of I to were significantly accelerated, indicating an open channel blocking action. The findings indicate that carvedilol significantly inhibits the major repolarization K+ currents I to and I Kur in human atrial myocytes. [Copyright &y& Elsevier]