Potassium Inhibits Dietary Salt-Induced Transforming Growth Factor- Production

Human and animal studies demonstrate an untoward effect of excess dietary NaCl (salt) intake on cardiovascular function and life span. The endothelium in particular augments the production of transforming growth factor (TGF), a fibrogenic growth factor, in response to excess dietary salt intake. This study explored the initiating mechanism that regulates salt-induced endothelial cell production of TGF. Male Sprague-Dawley rats were given diets containing different amounts of NaCl and potassium for 4 days. A bioassay for TGFdemonstrated increased (35.2%) amounts of active TGFin the medium of aortic ring segments from rats on the high-salt diet compared with rats maintained on a 0.3% NaCl diet. Inhibition of the large-conductance, calcium-activated potassium channel inhibited dietary salt-induced vascular production of TGFbut did not affect production of TGFby ring segments from rats on the low-salt diet. Immunohistochemical and Western analyses demonstrated the subunit of the calcium-activated potassium channel in endothelial cells. Increasing medium [K ] inhibited production of dietary salt-induced vascular production levels of total and active TGFbut did not alter TGFproduction by aortic rings from rats on the 0.3% NaCl diet. Increasing dietary potassium content decreased urinary active TGFin animals receiving the high-salt diet but did not change urinary active TGFin animals receiving the low-salt diet. The findings demonstrated an interesting interaction between the dietary intake of potassium and excess NaCl and further showed the fundamental role of the endothelial calcium-activated potassium channel in the vascular response to excess salt intake. (Hypertension. 2009;54:00-00.)