Apelin-13 deteriorates hypertension in rats after damage of the vascular endothelium by ADMA.

Asymmetric dimethylarginine (ADMA) is a risk factor for endothelial dysfunction. The polypeptide apelin has biphasic effects on blood vessels in vivo and in vitro. We investigated the effect of apelin-13 on ADMA-damaged vessels. Rats were divided among ADMA-treated and control groups, which were treated with ADMA (10 mg·(kg body mass)(-1)·day(-1)) or saline, respectively, for 4 weeks. Systolic blood pressure (SBP) was measured before and after the injection of apelin-13. The ultrastructure of endothelial cells in caudal arteries was examined using transmission electron microscopy. The reactivities of isolated caudal artery rings were observed after exposure to apelin-13, and myosin light chain (MLC) phosphorylation was assessed by immunohistochemistry in rings treated with or without apelin-13. ADMA induced hypertension and endothelial dysfunction. After injection of apelin-13, SBP declined in the control group but was elevated in the ADMA-treated group. In vitro, apelin-13 caused relaxation in rings in the control group, but it contracted rings in the ADMA-treated group. Apelin-13 promoted MLC phosphorylation in vascular smooth muscle cells (VSMCs) in the ADMA group. These results indicate that apelin-13 might pass through ADMA-damaged endothelium and act on VSMCs to increase MLC phosphorylation, thus contributing to vasoconstriction and exacerbating hypertension.

Improvement and influencing factors of blood pressure control by nephrologist referral in chronic kidney disease patients in China: a cohort study.

PURPOSE: Hypertension is an independent risk factor for mortality in chronic kidney disease (CKD) and is suboptimally controlled worldwide. Therefore, this study aimed to examine the rate of BP control and the main barriers to achieving target BP, according to K/DOQI guidelines, in China. METHODS: We performed a single-center, prospective cohort study. Two hundred and sixty CKD patients were referred by general physicians to nephrologists, and their BP was treated in accordance with K/DOQI guidelines for a 1-year follow-up. We evaluated improvement of BP target achievement and factors affecting BP control. We defined "not-at-goal" as persistence of systolic BP ≥ 130 mmHg and/or diastolic BP ≥ 80 mmHg after 1 year. RESULTS: The BP decreased from 138 ± 12/84 ± 7 mmHg at baseline to 124 ± 13/73 ± 7 mmHg after 1 year. The rate of achieving the BP goal (<130/80 mmHg) increased from 25.4 to 61.5 %. The decrease in BP was associated with a significant reduction of proteinuria (median, 0.14 vs 0.06 g/24 h; P < 0.05). Logistic regression analysis identified proteinuria levels ≥1.0 g/24 h (odds ratio [OR]: 5.21; 95 % confidence interval [CI]: 1.37-19.77) and high basal systolic BP (OR: 2.17; 95 % CI: 1.25-3.77) and diastolic BP (OR: 6.62; 95 % CI: 2.03-21.60) as independent predictors of not-at-goal BP. Higher educational level was independently associated with at-goal BP (OR: 0.21; 95 % CI: 0.06-0.78). CONCLUSIONS: In CKD patients, BP control is poor when managed by general physicians and may be improved after nephrologist referral. High basal BP and proteinuria levels ≥1.0 g/24 h are the main barriers that preclude the optimal control of BP.