In normal rabbits on a high-cholesterol diet we observed that reducing dietary potassium intake from normal (1.5%, plasma potassium concentration ϭ 4.3 mmol/L) to a low level (0.4%, plasma potassium concentration ϭ 3.9 mmol/L) increased the number of arteriosclerotic arteries in the myocardium by approximately 50%.1 More recently, we reported that elevation of dietary potassium intake reduced the severity of neointimal proliferative lesion formation in the arteries of rats and pigs after balloon angioplasty. 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. 4 -7 Growth factors released at the site by platelets, endothelial cells, white blood cells, and vascular smooth muscle cells stimulate migration of vascular smooth muscle cells from the media to the subintima, where they subsequently proliferate and synthesize extracellular matrix proteins. Migration to the point of injury is directed by platelet-derived growth factor BB (PDGF-BB), 8 -11 , whereas basic fibroblast growth factor (bFGF) and PDGF-BB are the prominent regulators of vascular smooth muscle cell proliferation. 6,8,9,12,13 Transforming growth factor beta 1 (TGF-1) stimulates synthesis of collagen and other extracellular matrix proteins by vascular smooth muscle cells in the subintima.5,14 The mechanism of the observed inhibition of arteriosclerotic lesion formation and neointimal proliferation by elevation of potassium intake may have included effects of extracellular potassium concentration on the release of these cytokines, or on their actions on vascular smooth muscle cell proliferation and migration.In this study we analyzed the effects of changes in extracellular potassium concentration in a physiologic range on the actions of PDGF-BB, bFGF, and 5% fetal bovine serum (5% FBS) to stimulate proliferation of vascular smooth muscle cells in vitro. The responses of vascular smooth muscle cells derived from explants of pig coronary arteries to the cytokines most important in the etiology of vascular lesions were assessed in media with potassium concentrations ranging from 3 to 6 mmol/L. Both DNA synthesis and cell proliferation were analyzed during changes in potassium concentration lasting from 1 to 7 days. MATERIALS AND METHODS Vascular Smooth Muscle Cell Isolation and CultureVascular smooth muscle cells were obtained from microdissected explants of the left circumflex coronary artery of castrated male,...
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