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Background and Objective: Apelin is a bioactive peptide manifesting a potent vasodilatory property. In this meta-analysis, we aimed to investigate for the first time whether circulating apelin differed significantly between hypertensive patients and normotensive controls.Methods: Both PubMed and Embase were searched for eligible articles. Eligibility evaluation and data collection were done independently by two investigators. Weighted mean difference (WMD) with 95% confidence interval (CI) was calculated under random-effects model by STATA.Results: Ten studies were synthesized finally, including 1610 patients and 1105 controls. Overall analysis revealed that circulating apelin was significantly lowered in patients than in controls (WMD = −39.85 pg/mL, 95% CI: −65.56 to −14.15; P = 0.002), with significant heterogeneity (I2= 89.4%). By race, patients had lower circulating apelin than controls in Caucasian populations (WMD = −79.82 pg/mL, 95% CI: −105.80 to −53.85; P < 0.001), without heterogeneity (I2=0.0%), while no significance was observed in Chinese and African-Americans. Further grouping studies by source of controls found a significant reduction in circulating apelin in studies with hospital-based controls (WMD = −96.28 pg/mL, 95% CI: −129.67 to −62.88; P < 0.001) (I2= 49.4%), but not in studies with population-based controls.Conclusions: Via a meta-analysis of 10 studies and on 2715 subjects, our findings demonstrated that lowered circulating apelin was significantly associated with an increased risk for hypertension, especially in Caucasian populations. [ABSTRACT FROM AUTHOR]

In the present study, we aimed to investigate the relationship of plasma matrix metalloproteinase-9 (MMP-9) and hematoma expansion (HE) in acute hypertensive cerebral hemorrhage (AHCH) (HE-in-AHCH). Patients with hypertensive cerebral hemorrhage, confirmed by head computed tomography (CT) within 12 h of onset, were prospectively collected. Venous blood was sampled within 4 h of the confirmation to determine the serum MMP-9 concentration. The blood pressure and National Institute of Health Stroke Score of the patients were recorded on hospital admission. CT re-scanning was performed within 42–54 h of the first head CT examination or immediately after worsening of the patients’ consciousness disorder. The relationship between MMP-9 level and HE was analyzed. A total of 186 patients were included. Of these patients, 41 had HE (22.0%). Multivariate logistic regression analysis showed that, in addition to the short interval between onset and the first CT examination, and the irregularity of hematoma shape, increasing MMP-9 level was an independent risk factor for HE-in-AHCH (OR value = 15.65, 95% CI: 5.30–46.15). Moreover, increasing plasma MMP-9 level was identified as an independent risk factor in patients with HE-in-AHCH. [ABSTRACT FROM PUBLISHER]

Background. To investigate the effects of a single dose of metformin (MF) on endothelium-dependent vasodilatation and serum antioxidant and free fatty acid levels in patients with primary hypertension (PH) after an acute glucose load. Materials and methods. Patients with untreated PH were randomized to a no-metformin group (PH, n = 34) and a metformin group (PH+ MF, n = 28) who received a single dose of 500 mg metformin before testing. Healthy volunteers ( n = 31) served as a control group. Brachial artery endothelium-dependent flow-mediated vasodilatation (FMD) was determined at 0, 1, 2 and 3 h after glucose load. Levels of serum superoxide dismutase (SOD), total antioxidant capacity (T-AOC), anti-superoxide anion free radical (AntiO2) and free fatty acids (FFA) were measured. Results. The FMD in the PH group decreased significantly 1 h after glucose load (PH: 10.9 ± 2.9% vs 13.67 ± 3.42% before glucose load). Metformin inhibited the effects of glucose load on FMD. At 1 h after acute glucose load, the concentrations of SOD, T-AOC and AntiO2 in the PH group decreased significantly compared with their fasting levels, and metformin inhibited the acute glucose load-induced decline in SOD and T-AOC levels. Conclusions. Metformin can prevent transient endothelial dysfunction caused by acute glucose load in patients with PH. [ABSTRACT FROM AUTHOR]