The most common cause of hypermagnesemia is impaired renal function. When the inulin clearance is less than 10 ml/min, the increase in magnesium excretion per nephron is insufficient to maintain a normal serum magnesium level. An unusual iatrogenic cause of hypermag-nesemia is due to the use of magnesium-containing urologic irrigation solutions for dissolution of urinary calculi. With higher serum magnesium concentrations, the hyporeflexia progresses to areflexia which precedes respiratory paralysis. This is why attention must be paid to testing the deep tendon reflexes during magnesium therapy. Excess magnesium affects the peripheral nervous system; it produces paralysis by suppressing the release of acetylcholine and blocking transmission at the neuromuscular junction. In the autonomic nervous system, magnesium excess also diminishes acetylcholine release and blocks transmission in sympathetic ganglia and in vagal terminals of the sino-atrial node. Magnesium appears to diminish the amount of transmitted substance released and it diminishes the sensitivity of the postsynaptic membrane to a given amount of the transmitter.