ABSTRACT
Patients with nondipper hypertension are known to carry a high risk of cardiovascular complications. Vitamin D deficiency is associated with hypertension. Because vitamin D deficiency activates the renin–angiotensin–aldosterone system (RAAS), we hypothesized that this vitamin would interact with the RAAS to influence blood pressure (BP) in nondipper hypertensive patients. We performed a cross-sectional analysis of 1,007 outpatients with hypertension (HTN). Dipper and nondipper patterns were detected, and the two groups were matched for clinical, laboratory, 25-hydroxyvitamin D (25OHD) levels, and ambulatory blood pressure recording. Plasma renin activity (PRA), angiotensin II, and plasma aldosterone concentration (PAC) were assessed in 174 patients treated with calcium channel blockers or no medication. The mean 25OHD concentration in the entire study population was 12.3ng/dL, and the prevalence of vitamin D deficiency was 87.0%. Dipper and nondipper HTN were noted in 187 patients (24.6%) and 573 patients (75.4%). 25OHD levels were similar between nondipper and dipper HTN groups. Forward stepwise logistic regression analysis showed that BMI and age were independent predictors of nondipper HTN. Neither 25OHD levels nor RAAS components were included in the model. In correlation analyses, nocturnal decline of diastolic BP was positively associated with 25OHD levels and standing PRA (r = 0.152 p = 0.045, r = 0.165 p = 0.038, respectively). The present study showed that vitamin D deficiency was astonishingly prevalent in hypertensive subjects residing in Xinjiang, China. There may be a weakly association of nocturnal DBP decline with 25OHD levels and standing PRA levels. We found no association between vitamin D deficiency and nondipper HTN.
Acknowledgments
The authors are grateful to Dr Nai-Wen Chi, Department of Medicine, University of California, San Diego, for his valuable support in modifying the language of the article.
Declaration of interest
The authors declare that they have no competing interests.
Funding
The present study was supported in part by grants from the State Key Lab Incubation Base of Xinjiang Major Disease Research (No: SKLIB-XJMDE-2014-1) to MCZ and the Natural Science Foundation of China (No: 81160038) to XJX.
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Notes on contributors
Xinjuan Xu
MCZ, HML, and HXL carried out epidemiologic survey, data analysis, and writing the article. MG and JSZ participated in epidemiologic survey. XJX and MCZ participated in the design of the study, performed the statistical analysis and modified the article. All authors commented on the article and approved the final version.