Enhanced Antioxidative Defense by Vitamins C and E Consumption Prevents 7-Day High-Salt Diet-Induced Microvascular Endothelial Function Impairment in Young Healthy Individuals

Abstract

This study aimed to examine whether the oral supplementation of vitamins C and E during a seven-day high salt diet (HS; ~14 g salt/day) prevents microvascular endothelial function impairment and changes oxidative status caused by HS diet in 51 (26 women and 25 men) young healthy individuals. Laser Doppler flowmetry measurements demonstrated that skin post-occlusive reactive hyperemia (PORH), and acetylcholine-induced dilation (AChID) were significantly impaired in the HS group, but not in HS+C+E group, while sodium nitroprusside-induced dilation remained unaffected by treatments. Serum oxidative stress markers: Thiobarbituric acid reactive substances (TBARS), 8-iso prostaglandin-F2α, and leukocytes’ intracellular hydrogen peroxide (H2O2) production were significantly increased, while ferric-reducing ability of plasma (FRAP) and catalase concentrations were decreased in the HS group. All these parameters remained unaffected by vitamins supplementation. Matrix metalloproteinase 9, antioxidant enzymes Cu/Zn SOD and glutathione peroxidase 1, and leukocytes’ intracellular superoxide production remained unchanged after the protocols in both HS and HS+C+E groups. Importantly, multiple regression analysis revealed that FRAP was the most powerful predictor of AChID, while PORH was strongly predicted by both FRAP and renin-angiotensin system activity. Hereby, we demonstrated that oxidative dis-balance has the pivotal role in HS diet-induced impairment of endothelial and microvascular function in healthy individuals which could be prevented by antioxidative vitamins consumption.

Mechanisms of Dietary Sodium-Induced Impairments in Endothelial Function and Potential Countermeasures

“…For instance, a high-sodium diet reduces the NO-mediated increase in skin blood flow in response to local heating in young, salt-resistant normotensive individuals [ 26 ]. In agreement with this finding, a high-sodium diet blunts the cutaneous blood flow response to ACh delivered via intradermal infusion [ 27 ] or iontophoresis [ 28 , 29 ]. Likewise, cutaneous post-occlusive reactive hyperemia is blunted in the absence of a change in BP following excess sodium consumption [ 28 , 30 ]; however, cutaneous reactive hyperemia appears to be mediated by endothelial release of prostaglandins rather than NO [ 30 , 31 ], and is beyond the scope of this review.…”

“…Likewise, Greaney et al demonstrated that local infusion of ascorbic acid restored the NO-mediated increase in skin blood flow to local heating in normotensive, salt-resistant individuals consuming excess sodium [ 26 ]. Oral supplementation with the antioxidant vitamins C and E during a high-sodium diet (5500 mg/day) similarly restored the skin blood flow response to cutaneous ACh iontophoresis while also preventing an increase in markers of oxidative stress in the plasma and urine [ 28 ].…”

Leukocyte Activation and Antioxidative Defense Are Interrelated and Moderately Modified by n-3 Polyunsaturated Fatty Acid-Enriched Eggs Consumption—Double-Blind Controlled Randomized Clinical Study

“…LDF measurements were performed in a temperature-controlled room. General procedures for performing LDF PORH test and LDF iontophoresis of ACh and SNP tests were done in accordance with our well-established protocols, which are described in detail in previous papers of our research group [ 18 , 19 , 20 ].…”

Is There Association between Altered Adrenergic System Activity and Microvascular Endothelial Dysfunction Induced by a 7-Day High Salt Intake in Young Healthy Individuals

“…We have earlier reported that in normotensive salt-resistant individuals' microvascular reactivity in response to vascular occlusion following 7-day HS diet was strongly predicted by both antioxidant capacity and the level of the RAS activity, rather than antioxidant capacity alone [18]. These results potentiated the key role of normal RAS function in maintaining vascular homeostasis and indicated that the alteration in RAS during dietary salt perturbation could be involved in concomitant changes in endothelial function [18].…”

“…We have earlier reported that in normotensive salt-resistant individuals' microvascular reactivity in response to vascular occlusion following 7-day HS diet was strongly predicted by both antioxidant capacity and the level of the RAS activity, rather than antioxidant capacity alone [18]. These results potentiated the key role of normal RAS function in maintaining vascular homeostasis and indicated that the alteration in RAS during dietary salt perturbation could be involved in concomitant changes in endothelial function [18]. Since the SNS activity presents a significant regulator of the RAS activation, it became evident that in order to clarify the pathogenic relation between HS diet and impaired vascular function, it is necessary to investigate the effect of salt loading on major regulating systems, including RAS and autonomic nervous system (ANS) activity, in otherwise healthy individuals.…”