The effect of a high potassium diet on microvascular function under high sodium conditions in healthy adults

Abstract

Excess sodium intake is a major contributor to cardiovascular disease risk. Beyond its effects on blood pressure (BP), excess sodium intake induces endothelial dysfunction, an important precursor to atherosclerosis. A high sodium diet is also shown to impair microvascular function, an effect mediated by oxidative stress. We have shown that a high potassium diet effectively counteracts sodium-induced endothelial dysfunction of a conduit artery in healthy adults, independent of BP. Our objective was to explore the effect of a high potassium diet on microvascular function in the context of a high sodium diet. We hypothesized microvascular function would improve on a high potassium/high sodium (HK/HS) diet compared to a moderate potassium/high sodium (MK/HS) diet, and these effects would be mediated by oxidative stress. Thirty-three healthy, salt-resistant adults (18 men, 19 women; aged 32 ± 12 y; BMI 24.3 ± 2.5 kg/m2; BP 113 ± 19/72 ± 11 mmHg) consumed two controlled diets for seven days in random order: MK/HS (65 mmol/300 mmol) and HK/HS (120 mmol/300 mmol). On day seven of each diet, four intradermal microdialysis fibers were inserted in the ventral side of the left forearm for the perfusion of lactated Ringer’s, 20 μM ascorbic acid, 100 μM apocynin, and 10 μM TEMPOL. Red blood cell flux in response to local heating was measured via laser doppler flowmetry, and BP was measured throughout the protocol. After achieving a plateau at 42°C, 10 μM L-NAME was perfused to quantify nitric oxide (NO) contribution to vasodilation. Temperature was then increased to 43°C and 28 μM sodium nitroprusside was perfused to achieve maximal vasodilation. Cutaneous vascular conductance (CVC) during each phase was calculated by dividing red blood cell flux by mean arterial pressure. Results are reported as %CVCmax. Within each phase of the protocol, differences in %CVCmax at the lactated Ringer’s site on the MK/HS vs. HK/HS diet were compared via paired samples t-tests, and differences among all four microdialysis sites within each diet were compared via repeated measures ANOVA. There were no differences in the baseline %CVCmax at the lactated Ringer’s site between the MK/HS and HK/HS diets (18.6 ± 15.4 %CVCmax vs. 17.0 ± 13.2 %CVCmax, p=0.51). There were no differences in the plateau %CVCmax at the lactated Ringer’s site between the MK/HS and HK/HS diets (87.6 ± 10.7 %CVCmax vs. 87.1 ± 9.5 %CVCmax, p=0.82). Ascorbic acid, apocynin, and TEMPOL had no effect on the plateau %CVCmax on either diet, and did not affect the NO contribution (all p>0.05). These findings suggest potassium may not improve microvascular function in the context of a high sodium diet in healthy, salt-resistant adults. These findings should be confirmed to fully elucidate the effects of sodium and potassium on microvascular function. R01 HL145055, P20GM113125 This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.