The forestomach is the main site of Mg2+ absorption in the gastrointestinal
tract of ruminants and maintains Mg2+ homeostasis. It has long been known
that an increase in K+ intake and, consequently, in ruminal K+ concentratio
n ([K+]) decreases the apparent digestibility of Mg2+, which increases the
risk of hypomagnesemia and tetany.
The present review summarizes new findings on the mechanisms of Mg2+ absorp
tion across the rumen epithelium. It has been shown that transcellular and
active Mg2+ transport is the predominant pathway for Mg2+ transport from lu
men to blood. It is well established that the apical uptake of Mg2+ is medi
ated by a PD-independent or K+-insensitive and by a parallel working PD-dep
endent, K+ sensitive mechanism. The predominant driving force for the elect
rodiffusive Mg2+ uptake is PDa, the potential difference across the apical
membrane of the rumen epithelium, that amounts to -50 mV under physiologica
l conditions, permitting an effective Mg2+ absorption even at very low lumi
nal Mg2+ concentrations. The antagonism between K+ and Mg2+ absorption can
be explained by K+ dependent electrophysiological changes of the rumen epit
helium. An elevation of the ruminal [K+] has two different effects that are
responsible for the observed reduction of net Mg2+ absorption; (1) It depo
larizes PDa and thereby reduces the driving force for the electrodiffusive
Mg2+ uptake into the ruminal epithelial cells, hence decreases the cytosoli
c [Mg2+] and the transcellular component of Mg2+ absorption; (2) It increas
es the transepithelial potential difference (PD,; blood-side positive) and,
hence causes a small, passive backflow of Mg2+ via the paracellular route
from the blood side into the lumen.
The second, PD-independent uptake mechanism is primarily working at high ru
minal [Mg2+]. Therefore the negative effect of K+ can be compensated by thi
s K+ insensitive Mg2+ absorption, if high [Mg2+] are present in the ruminal
fluid.