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Original Articles

Nocturnal diastolic blood pressure decline is associated with higher 25-hydroxyvitamin D level and standing plasma renin activity in a hypertensive population

, , , , &
Pages 685-690 | Received 31 Aug 2016, Accepted 21 Nov 2016, Published online: 05 Sep 2017
 

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.

Additional information

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.

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.

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