Wellington Medical Technology Group, Department of Surgery and Anaesthesia, University of Otago, Wellington, New Zealand.
Centre for Translational Physiology, University of Otago, Wellington, New Zealand.
J Appl Physiol (1985). 2019 Sep 1;127(3):760-769. doi: 10.1152/japplphysiol.01116.2018. Epub 2019 Jul 18.
Insufficient nitric oxide (NO) bioavailability plays an important role in endothelial dysfunction, and increased NO has the potential to enhance cerebral blood flow (CBF). Dietary supplementation with sodium nitrate, a precursor of NO, could improve cerebrovascular function, but this has not been investigated. In 17 individuals, we examined the effects of a 7-day supplementation of dietary nitrate (0.1 mmol·kg·day ) on cerebrovascular function using a randomized, single-blinded placebo-controlled crossover design. We hypothesized that 7-day dietary nitrate supplementation increases CBF response to CO (cerebrovascular CO reactivity) and cerebral autoregulation (CA). We assessed middle cerebral artery blood velocity (MCAv) and blood pressure (BP) at rest and during CO breathing. Transfer function analysis was performed on resting beat-to-beat MCAv and BP to determine CA, from which phase, gain, and coherence of the BP-MCAv data were derived. Dietary nitrate elevated plasma nitrate concentration by ~420% ( < 0.001) and lowered gain ( = 1.2, = 0.025) and phase of the BP-MCAv signal compared with placebo treatment ( = 0.7, = 0.043), while coherence was unaffected ( = 0.122). Dietary nitrate increased the MCAv-CO slope in a sex-specific manner (interaction: = 0.016). Dietary nitrate increased the MCAv-CO slope in men ( = 1.0, = 0.014 vs. placebo), but had no effect in women ( = 0.919). Our data demonstrate that dietary nitrate greatly increased cerebrovascular CO reactivity in healthy individuals, while its effect on CA remains unclear. The selective increase in the MCAv-CO slope observed in men indicates a clear sexual dimorphic role of NO in cerebrovascular function. We found dietary nitrate supplementation improved the brain blood vessels' response to CO, cerebrovascular CO reactivity, without affecting blood pressure in a group of healthy individuals. Meanwhile, the effect of dietary nitrate on the relationship between blood pressure and brain blood flow, cerebral autoregulation, was inconclusive. The improvement in cerebrovascular CO reactivity was only observed in the male participants, alluding to a sex difference in the effect of dietary nitrate on brain blood flow control. Our findings indicate that dietary nitrate could be an effective strategy to enhance cerebrovascular CO reactivity.
一氧化氮（NO）生物利用度不足在血管内皮功能障碍中起重要作用，增加 NO 有可能增强脑血流（CBF）。饮食补充 NO 的前体硝酸钠可能改善脑血管功能，但这尚未得到研究。在 17 名个体中，我们使用随机、单盲安慰剂对照交叉设计研究了 7 天饮食硝酸盐补充对脑血管功能的影响。我们假设 7 天饮食硝酸盐补充增加了 CO 对 CBF 的反应（脑血管 CO 反应性）和脑自动调节（CA）。我们在休息和 CO 呼吸期间评估大脑中动脉血流速度（MCAv）和血压（BP）。在休息时对 MCAv 和 BP 进行逐拍传递函数分析，以确定 CA，从中得出 BP-MCAv 数据的相位、增益和相干性。饮食硝酸盐使血浆硝酸盐浓度升高约 420%（ < 0.001），并降低了 BP-MCAv 信号的增益（ = 1.2， = 0.025）和相位（ = 0.7， = 0.043），而相干性不受影响（ = 0.122）。饮食硝酸盐以性别特异性方式增加 MCAv-CO 斜率（交互作用： = 0.016）。饮食硝酸盐增加了男性的 MCAv-CO 斜率（ = 1.0， = 0.014 与安慰剂相比），但对女性没有影响（ = 0.919）。我们的数据表明，饮食硝酸盐在健康个体中大大增加了脑血管对 CO 的反应性，而其对 CA 的影响尚不清楚。在男性中观察到的 MCAv-CO 斜率的选择性增加表明，NO 在脑血管功能中具有明显的性别二态作用。我们发现，在一组健康个体中，饮食硝酸盐补充改善了血管对 CO 的反应，即脑血管 CO 反应性，而不影响血压。同时，饮食硝酸盐对血压与脑血流、脑自动调节之间关系的影响尚无定论。MCAv-CO 反应性的改善仅在男性参与者中观察到，这暗示了饮食硝酸盐对脑血流控制的影响存在性别差异。我们的研究结果表明，饮食硝酸盐可能是增强脑血管 CO 反应性的有效策略。
