High potassium intake inhibits neointima formation in the rat carotid artery balloon injury model

Abstract

Recently, we reported that elevated extracellular potassium concentration in vitro inhibited proliferation and migration of vascular smooth muscle cells, formation of free radical compounds by macrophages, and reduced platelet sensitivity to agonists. In the present study we analyzed the effects of long-term, in vivo elevation of extracellular potassium concentration resulting from changes in dietary potassium intake on the vascular response to injury. The rat carotid artery balloon injury model was employed in 70 adult Sprague Dawley rats assigned to three groups. Beginning 14 days before surgical placement of the carotid lesion and continuing until death, the animals were fed diets containing either low (0.1% potassium, n = 25), normal (1.5% potassium, n = 19), or high potassium (4.0% potassium, n = 26). Fourteen days postsurgery the animals were killed and the arteries were analyzed to determine quantitatively the ratio of neointimal to medial area. Dietary potassium had a significant effect on arterial plasma potassium concentration (one-way analysis of variance, P < .01). Group mean and standard errors were 4.26+/-0.12 mmol/L for the low-potassium group, 5.22+/-0.19 mmol/L for normal, and 5.80+/-0.23 mmol/L for the high-intake group. Increases in dietary potassium attenuated neointima formation significantly (P < .05, one-way analysis of variance), with the mean ratio of neointimal area to medial area being 0.447+/-0.106 for the low-intake animals, 0.384+/-.116 for normal, and 0.240+/-.046 for the high-intake group. These results are consistent with a hypothesis that a high level of potassium intake is effective in inhibiting neointima formation in vivo.

Dietary potassium regulates vascular calcification and arterial stiffness

“…In animal models, elevation of extracellular potassium levels resulting from increased dietary potassium intake attenuated balloon injury-induced neointimal formation in rat carotid arteries, possibly through inhibition of proliferation and migration of VSMCs (27). In a population-based study, high levels of dietary potassium have been postulated to impair proliferation of VSMCs, and reduce monocyte adherence to vessel walls, thereby retarding the progression of atherosclerosis (28).…”

Protective Effect of Dietary Potassium Against Vascular Injury in Salt-Sensitive Hypertension

“…It has been speculated that this may be a result of the vasoprotective effect of potassium, because potassium supplementation has been shown to ameliorate vascular endothelial dysfunction in salt-loaded DS rats. 3 Also, Ma et al 4 clearly demonstrated that high-potassium intake inhibited neointimal formation in several vascular injury models, such as a balloon injury of rat carotid and swine coronary 5 arteries from animals without hypertension. Thus, dietary potassium may have vasoprotective mechanisms beyond the blood pressure (BP)-lowering effect.…”

Increased potassium concentration inhibits stimulation of vascular smooth muscle proliferation by PDGF-BB and bFGF

“…Suppression of these functions could be responsible in part for the reduction in formation of arteriosclerotic and neointimal proliferative lesions observed in animals given high potassium diets. [1][2][3] …”

“…In the study in normal adult rats, increasing potassium in the diet from a low level (0.1%) to a high level (4.0%) reduced the neointimal to medial area ratio by 46%, in association with an increase in plasma potassium concentration from 4.3 to 5.8 mmol/L. 2 In the coronary artery of pigs after balloon angioplasty, the neointimal to medial area ratio was reduced by 45% in association with an increase in dietary potassium intake from 0.25% (plasma potassium concentration ϭ 3.1 mmol/L) to 2.0% (plasma potassium concentration ϭ 4.0 mmol/L). The etiology of formation of both the arteriosclerotic lesion and the neointimal proliferative lesion associated with angioplasty have been studied extensively.…”