Release of antidiuretic hormone during mass-induced elevation of intracranial pressure

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Abstract
There are complex osmotic and non-osmotic factors regulating release of antidiuretic hormone (ADH). A wide variety of intracranial pathological processes may trigger ADH release sufficient to produce clinically recognizable hyponatremia, or the inappropriate ADH syndrome. One non-osmotic trigger, i.e., mass-induced elevated intracranial pressure (ICP), was systematically studied. Initial experiments established baseline data in normal rhesus monkeys: anesthetized animals displayed appropriate rises and falls in immunoreactive urinary ADH in response to i.v. administered hypertonic and hypotonic infusions. Next, balloon catheters were implanted subdurally over temporal lobes, and the animals were allowed to recover. The final experiment consisted of anesthetizing the animals, monitoring arterial blood pressure and blood gases, and retrieving timed urinary specimens while continuously recording ICP during infusion-pump expansion of the subdural balloon. A nonlethal and a lethal series of balloon-expansion experiments were done. Control values of urinary ADH were 783 .+-. 125 .mu.U[microunits]/15 min, and ICP was less than 10 mm Hg. During nonlethal mass expansion ADH output rose to 3433 .+-. 269 .mu.U/15 min, while ICP averaged 65 mm Hg (measured at completion of mass expansion). While the mass was maintained, hypotonic infusion produced unchanged urinary ADH output of 3452 .+-. 277 .mu.U/15 min. During lethal experiments, urinary ADH rose still higher to 4339 .+-. 1887 .mu.U/15 min associated with ICP averaging 100 mm Hg. There is a direct relationship between the magnitude of ICP and the amount of ADH release, and during elevated ICP the ADH release is not suppressed by hypotonic infusion.