Potassium Inhibits Dietary Salt-Induced Transforming Growth Factor-β Production
- 1 November 2009
- journal article
- research article
- Published by Ovid Technologies (Wolters Kluwer Health) in Hypertension
- Vol. 54 (5), 1159-1163
- https://doi.org/10.1161/HYPERTENSIONAHA.109.138255
Abstract
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)-β, 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-β. Male Sprague-Dawley rats were given diets containing different amounts of NaCl and potassium for 4 days. A bioassay for TGF-β demonstrated increased (35.2%) amounts of active TGF-β in 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 TGF-β but did not affect production of TGF-β by ring segments from rats on the low-salt diet. Immunohistochemical and Western analyses demonstrated the α 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 TGF-β but did not alter TGF-β production by aortic rings from rats on the 0.3% NaCl diet. Increasing dietary potassium content decreased urinary active TGF-β in animals receiving the high-salt diet but did not change urinary active TGF-β in 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.Keywords
This publication has 34 references indexed in Scilit:
- Joint Effects of Sodium and Potassium Intake on Subsequent Cardiovascular DiseaseArchives of Internal Medicine, 2009
- Molecular mechanisms of BK channel activationCellular and Molecular Life Sciences, 2008
- Mechanism of dietary salt-mediated increase in intravascular production of TGF-β1American Journal of Physiology-Renal Physiology, 2008
- Long term effects of dietary sodium reduction on cardiovascular disease outcomes: observational follow-up of the trials of hypertension prevention (TOHP)BMJ, 2007
- Emilin1 Links TGF-β Maturation to Blood Pressure HomeostasisCell, 2006
- Decreased Expression of Maxi-K + Channel β 1 -Subunit and Altered Vasoregulation in HypoxiaCirculation, 2005
- Modest Salt Reduction Reduces Blood Pressure and Urine Protein Excretion in Black HypertensivesHypertension, 2005
- Dietary salt intake activates MAP kinases in the rat kidney 1The FASEB Journal, 2002
- Increased dietary salt accelerates chronic allograft nephropathy in ratsKidney International, 2001
- Salt Sensitivity, Pulse Pressure, and Death in Normal and Hypertensive HumansHypertension, 2001