Abstract

Background and Aim: The association of habitual intakes of dietary nitrate (NO3−) and nitrite (NO2−) with blood pressure and renal function is not clear. Here, we investigated a potential effect of dietary NO3− and NO2− on the occurrence of hypertension (HTN) and chronic kidney disease (CKD). Methods: A total of 2799 Iranian adults aged ≥20 years, participating in the Tehran Lipid and Glucose Study (TLGS), were included and followed for a median of 5.8 years. Dietary intakes of NO3− and NO2− were estimated using a semi-quantitative food frequency questionnaire. Demographics, anthropometrics, blood pressure and biochemical variables were evaluated at baseline and during follow-up examinations. To identify the odds ratio (OR) and 95% confidence interval (CI) of HTN and CKD across tertile categories of residual energy-adjusted NO3− and NO2− intakes, multivariate logistic regression models were used. Results: Dietary intake of NO3− had no significant association with the risk of HTN or CKD. Compared to the lowest tertile category (median intake < 6.04 mg/day), the highest intake (median intake ≥ 12.7 mg/day) of dietary NO2− was accompanied with a significant reduced risk of HTN, in the fully adjusted model (OR = 0.58, 95% CI = 0.33–0.98; p for trend = 0.054). The highest compared to the lowest tertile of dietary NO2− was also accompanied with a reduced risk of CKD (OR = 0.50, 95% CI = 0.24–0.89, p for trend = 0.07). Conclusion: Our findings indicated that higher intakes of NO2− might be an independent dietary protective factor against the development of HTN and CKD, which are major risk factors for adverse cardiovascular events.

Highlights

  • Elevated blood pressure and renal dysfunction represent world-wide public health problems and are known to be major underlying causes for cardiovascular disease morbidity and mortality [1,2].The key role of disrupted nitric oxide (NO) pathway, including either decreased production or reduced bioavailability of NO, is well established in the pathogenesis of hypertension (HTN) and kidneyNutrients 2016, 8, 811; doi:10.3390/nu8120811 www.mdpi.com/journal/nutrientsNutrients 2016, 8, 811 disease [3,4,5]

  • Dietary intakes of NO2 − from animal sources accounted for 42.4% of daily mean intake of NO2 − and the remainder of NO2 − intake was derived from plant sources

  • We investigated the potential impact of habitual dietary NO3 − and

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Summary

Introduction

Elevated blood pressure and renal dysfunction represent world-wide public health problems and are known to be major underlying causes for cardiovascular disease morbidity and mortality [1,2].The key role of disrupted nitric oxide (NO) pathway, including either decreased production or reduced bioavailability of NO, is well established in the pathogenesis of hypertension (HTN) and kidneyNutrients 2016, 8, 811; doi:10.3390/nu8120811 www.mdpi.com/journal/nutrientsNutrients 2016, 8, 811 disease [3,4,5]. Elevated blood pressure and renal dysfunction represent world-wide public health problems and are known to be major underlying causes for cardiovascular disease morbidity and mortality [1,2]. The key role of disrupted nitric oxide (NO) pathway, including either decreased production or reduced bioavailability of NO, is well established in the pathogenesis of hypertension (HTN) and kidney. Considering the role of NO as the key regulator of vascular homeostasis and natural vasodilator, supplementation with inorganic NO3 − and NO2 − have been investigated as potential therapeutic options in cardiovascular disease, including HTN, and in states renal dysfunction [23,24,25,26]. We investigated a potential effect of dietary NO3 − and NO2 − on the occurrence of hypertension (HTN) and chronic kidney disease (CKD).

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