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

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." We systematically studied one non-osmotic trigger, namely mass-induced elevated intracranial pressure (ICP). Initial experiments established baseline data in normal rhesus monkeys: anesthetized animals displayed appropriate rises and falls in immunoreactive urinary ADH in response to intravenously administered hypertonic and hypotonic infusions. Next, ballon catherters were implanted subdurally over temporal lobes and the animals were allowed to recover. The final experiment consisted of anethetizing 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 ballon. A nonlethal and a lethal series of ballon-expansion experiments were done. Control values of urinary ADH were 783 +/- 125 muU/15 min, and ICP was less than 10 mm Hg. During nonlethal mass expansion ADH output rose of 3433 +/- 269 millimicronU/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 muU/15 min. During lethal experiments, urinary ADH rose still higher to 4339 +/- 1887 muU/15 min associated with ICP averaging 100 mm Hg. We concluded that there is a direct relationship between the magnitude of ICP and the amount of ADH release, and that during elevated ICP the ADH release is not suppressed by hypotonic infusion.