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The ruminal epithelium is a stratified squamous epithelium that has evolved to display functions essential for the unique ability of cows and sheep to ferment dietary components like carbohydrates and protein, and to selectively absorb nutrients and minerals for the production of milk. A characteristic property of this tissue is its pronounced ability to transport magnesium against an electrochemical gradient. Absorption of magnesium is reduced by dietary elevation of ruminal potassium, leading to hypomagnesaemia that can reach clinical significance. Studies of the intact tissue and of isolated cells suggest that cellular magnesium uptake is decreased by apical depolarization of the ruminal membrane, resulting in both a lower cytosolic concentration and transepithelial transport of the element.
Another characteristic feature of this unusual epithelium is the expression of a sodium-conducting channel with functional properties that are clearly distinct from the epithelial sodium channel (ENaC) found in most mammalian epithelia. Thus, it has not been possible to demonstrate direct regulation of ruminal sodium transport by aldosterone, and the effects of amiloride are clearly limited to an inhibition of the sodium proton exchanger (NHE3) expressed by this tissue. Studies at the level of the animal and the tissue suggest that sodium conductance is enhanced by depolarization of the apical membrane. Recent in vitro studies have demonstrated that ruminal epithelial cells express non-selective cation channels in the apical membrane that are regulated by changes in cytosolic magnesium. We propose that the reduction in ruminal magnesium uptake observed after ingestion of high potassium fodder may be related to a role for magnesium in a signaling cascade that leads to an increase in the permeability of this non-selective cation channel for sodium, thus enhancing absorption of this ion from the rumen and restoring ruminal osmolarity, while contributing to the retention of potassium.