Speculations on hormonal controls of magnesium homeostasis: a hypothesis

Magnesium deficiency (MD) may be either latent: i.e. without disturbances in blood Mg, calcium and intracellular potassium (Ki) or patent, with a rich symptomatology: i.e. with hypomagnesemia, hypocalcemia and decreased Ki. These two aspects are also found with magnesium excess. The discrepancy between these two opposite clinical forms leads one to postulate the existence of a control of Mg homeostasis, efficient in latent forms and deficient in patent forms of Mg disturbances. 4 'endocrine glands', (i.e.) adrenal medulla, parathyroids, thyroid and beta-islets in the pancreas are involved mainly in the homeostatic feed-back systems which regulate both Mg levels and the humoral consequences of the disturbances of Mg metabolism. Moreover, the high stability of intracellular Mg2+ in soft tissues also leads one to postulate the existence of cellular feedback regulatory mechanisms. Parallel variations of insulin and epinephrine secretion represent the first known mechanism which tends to maintain constancy of cellular Mg2+, and, secondarily, of 3':5'-cyclic adenosine monophosphate (cAMP). However, this regulation involves 3 types of side effects; i.e. in MD, the epinephrine-insulin hypersecretion may induce: membrane-depolarizing effects, calcinosis-promoting increase of cellular P and Ca influx, and an increase of the 3':5'-cyclic guanosine monophosphate (cGMP) level--the basic characteristics of cellular MD. These noxious side effects may be antagonized by an increase of taurine (TA) influx into the cell, which is actually stimulated by epinephrine-insulin hypersecretion. TA--and perhaps also gamma-L-glutamyl TA, new parathyroid hormone--may counteract all of these side effects by its membrane-stabilizing, Ca-binding and cGMP level-lowering effects. TA, through these nonspecific functions, and perhaps also through a specific action as an 'Mg-sparing hormone', thus appears to be an important factor in the regulation of Mg homeostasis.