Dietary Potassium Attenuates the Effects of Dietary Sodium on Vascular Function in Salt‐Resistant Adults

Abstract

Cardiovascular disease remains a major public health problem in the U.S. and is the result of lifestyle factors, such as nutrition, that play an important role. Excess sodium consumption can increase blood pressure (BP) while consumption of potassium has been shown to have BP lowering properties. While the effect of these two nutrients on BP is fairly well understood, their impact on vascular function, particularly any interactive effects, has received less attention. Endothelial dysfunction, characterized by impaired dilation, is an important non‐traditional risk factor for atherosclerosis. Therefore, the purpose of this study was to determine if dietary potassium can offset the deleterious effect of high sodium on endothelial function as assessed by brachial artery flow‐mediated dilation (FMD). Thirty‐three adults with salt‐resistant BP (16M,17F; 27±1yr) completed 7 days each of the following diets: 65 mmol potassium/50 mmol sodium (MK/LS); 65 mmol potassium/300 mmol sodium (MK/HS); and 120 mmol potassium/300 mmol sodium (HK/HS) in random order. On the last day of each diet, 24‐hour ambulatory BP, 24‐hour urine collection and a blood draw was performed. FMD was assessed in response to reactive hyperemia. 24‐hr BP did not differ between diets confirming that subjects were salt‐resistant. Sodium excretion increased on both HS diets compared to LS/MK (p<0.05) and potassium excretion was increased on the HK diet compared to MK/LS and MK/HS (p<0.05) confirming diet compliance. Aldosterone and plasma renin activity were elevated on MK/LS compared to both HS diets (p<0.05). FMD was impaired on MK/HS (5.4±0.5%) compared to both MK/LS (7.0±0.6%; p<0.05) and HK/HS (6.5±0.5%; p<0.05) while there was no difference between the MK/LS and HK/HS diets (p>0.05). These data suggest that potassium provides vascular protection against the deleterious effects of high sodium on conduit artery function. Support or Funding Information This work was supported by NIH NIGMS grant # P20GM113125.

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

“…In a subset of subjects, nitroglycerin induced similar dilation of the brachial artery across both diets, providing evidence that the impairment occurred at the endothelium [ 37 ] and not the VSM cells. High dietary sodium-induced reductions in FMD have been found in multiple [ 30 , 38 ] but not all [ 27 ] studies. There is some evidence that the impact of a high-sodium diet on FMD is greater in men than women [ 39 ].…”

“…Sundhir and colleagues also observed a protective effect of potassium supplementation (2.1% potassium chloride or 2.1% potassium bicarbonate) against the vascular insult of sodium in Dahl rats; however, these findings appeared to be related to a direct effect of potassium on systolic BP [ 108 ]. Notably, in young, salt-resistant humans, a high-potassium diet (4700 mg/day) abolished the reduction in brachial artery FMD caused by a seven-day high-sodium diet with moderate potassium intake (2500 mg/day), despite no change in either laboratory-measured or 24-hr ambulatory BP [ 38 ]. Furthermore, added dietary potassium counteracts an acute sodium insult without changing BP, as the postprandial reduction in FMD following a single high-sodium meal containing only 117 mg of potassium was completely abolished when the high-sodium meal contained 1482 mg of potassium [ 43 ].…”