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Objective The purpose of this study was to explore the protective effects of telmisartan and pyridoxamine on tubular epithelial cells (HK-2) in early renal damage. Methods Cultured HK-2 cells were divided into HK-2 control, angiotensin II (10−6 mol/l) group (Ang II), telmisartan (10−6 mol/l, T) group, pyridoxamine group (1 mmol/l, P1), pyridoxamine group (10 mmol/l, P10), and T (10−6 mol/l)+P (10 mmol/l) group (T+P). Methyl thiazolyl tetrazolium (MTT) was used to measure for cell proliferation. Reactive oxygen species (ROS) generation in cellular supernatant was detected by flow cytometry. Real-time quantitative PCR was performed to measure the mRNA expression of transforming growth factor β1 (TGFβ1) and receptor for advanced glycation end-products (RAGE). Results The OD values of HK-2 were inhibited in Ang II (p 0.05). Compared with the Ang II, mRNA expression of RAGE and TGFβ1 were decreased in T, P and TP group (p

Objective To investigate the effects of telmisartan and pyridoxamine on vascular smooth muscle cells (VSMCs) proliferation and apoptosis with abdominal aorta vascular remodelling in spontaneously hypertensive rat (SHR). Methods SHR randomly received hypertensive, telmisartan (6 mg/kg/d), pyridoxamine (200 mg/kg/d) or combination therapy (telmisartan 6 mg/kg/d, pyridoxamine 200 mg/kg/d). Drug treatment lasted for 16 weeks. Wistar-Kyoto (WKY) as control. The systolic blood pressure (SBP) of rat was measured before and after experimentation every weeks. The serum advanced glycation end-products (AGEs) were detected by competitive ELISA. The serum super oxide dismutase (SOD), nitric oxide (NO) were measured chemical method. The abdominal aorta were assessed by image analysis in HE stained sections. The VSMCs apoptosis and proliferation in abdominal aorta were detected with in situ end labelling technique and proliferating cell nuclear antigen (PCNA) immunohistochemistry staining, respectively. Results The levels of SBP were significantly lower in telmisartan and combination therapy treated SHR than that in hypertensive rats. There was no significant difference between pyridoxamine and WKY (p>0.05). The activity of SOD and NO were significantly higher and AGEs significantly lower in telmisartan, pyridoxamine and combination therapy treated SHR than that in hypertensive rats (p Conclusion Telmisartan and pyridoxamine could partial synergistically improved the blood remodelling associated with attenuation in oxidative stress status and improve the VSMCs unbalance relationship of proliferation and apoptosis in SHR abdominal aorta. Telmisartan was also associated with significant reducing blood pressure.

Objective The authors explore the relationship between the serum uric acid levels and blood pressure (BP) response to antihypertensive drugs treatment in male hypertensives by a hospitalisation-based retrospective analysis. Methods According to serum uric acid (SUA) levels, 804 male inpatients with diagnosis of hypertension were divided into two groups, the hyperuricaemia patients (SUA>420 μmol/l, n=305) and patients with normal SUA levels (SUA Result The hypertensive patients with hyperuricaemia have higher body mass index (BMI), dyslipidaemia ratio, systolic BP (diastolic BP), serum creatinine, antihypertensive therapeutic intensity score (p Conclusions The results suggest that serum uric acid levels could affect blood pressure response to the antihypertensive therapy in male hypertensives.

Objective To investigate the influence of pyridoxamine on the pre- iferation of rat vascular smooth muscle cells induced by Angiotensin (A)in vitro and its mechanism. Methods Primary VSMCs were cultivated from the thoracic aortas of spontaneously hypertensive rats, and which from the 3th to 5th generation at exponential phase of growth were selected for the experiments and induced by A (10 −7 mol/l). The proliferation of VSMCs after intervention with pyridoxamine (0.1, 1 and 10 mmol/l) was determined by MTT. The levels of advanced glycation end-products in cellular supernatant was determined by enzyme-linked immunosorbent assay (ELISA) and the intracellular level of reactive oxygen species (ROS) was detected by f1ow cytometry. The mRNA expressions of RAGE, NF-κB-P65, NADPH oxidaseP47phox were detected by Real-time PCR. Results The proliferation of VSMCs induced by A was inhibited by pyridoxamine in dependent-concentration manner (0.1, 1 and 10 mmol/l). The cellular supernatant AGEs level in pyridoxamine (1 mmol/l, P1) and pyridoxamine (10 mmol/l, P10) group was significantly lower (p Conclusions The pyridoxamine inhibits the proliferation of VSMCs induced by A in dependent-concentration manner, and the potential mechanism of which pyridoxamine may reduce the expressions of RAGE by NF-κB pathway signals and inhibiting AGEs expressing and oxidative stress.

Objective To explore the relationship between ankle-brachial index (ABI) and atherosclerosis in patients with non-dialysis chronic kidney disease (CKD). Method As a cross-sectional study, 118 patients with diagnosis of non-dialysis CKD (stage 1–5) were selected in our hospital from October 2008 to October 2009. Clinical data were recorded, including sex, age, height, weight, smoking status, blood pressure (BP), fasting glucose, high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C) and renal function. eGFR was calculated by modification of diet in renal disease study equation. ABI values were determined with a Doppler prober. ANOVA, bivariate correlation analysis and multiple linear regression were used for statistical analysis. Results According to eGFR, all patients were divided into five groups as CKD stage 1 group to CKD stage 5 group. There were significant differences in ABI value between five groups (F=28.123, p 0.05). ABI value was significantly decreased with gradual decline of eGFR level (p Conclusion Renal dysfunction is an independent risk factor for atherosclerosis. Decline of eGFR was closely related with the degree of atherosclerotic lesions. ABI can be used as important clinical indicators of atherosclerosis in patients with CKD.