Control of Release of ADH and its Disturbance

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It is well known that hemorrhage and plasma hypertonicity cause release of antidiuretic hormone (ADH) from neurohypophysis. Levels of ADH in jugular vein plasma were measured by the method of Yoshida et al. in order to elucidate location of the pathways through which osmotic or hemorrhagic stimuli influences neurohypophysis. The following experiments were performed before and after saline infusion or hemorrhage. In intact dogs, hemorrhage caused massive increase in ADH levels in plasma. Decerebrated dogs and dogs with diencephlic islands did not show any significant response after hemorrhage. Decorticated dogs and dogs with their spinal cord sectioned at the level of C-1 showed good responses. Dogs with cervical vagus nerves sectioned showed significantly weaker responses than that of intact dogs or dogs with abdominal vagus nerves sectioned. Hypertonic saline infusion caused a significant increase in ADH level in intact dogs and also in dogs with diencephalic islands. These results suggested location of the receptor for osmotic stimulus in the diencephalon, while vagal afferents arising from the thoracic cavity contribute intimately to the massive release of ADH after hemorrhage. The degree of increase in plasma ADH level was examined after the maximal osmotic stimulus produced by infusion of 10% or 30% saline solution and after subsequent hemorrhage. The ADH levels in plasma after infusion of hypertonic saline were 12% of the levels after hemorrhage, which suggests that the ADH releasing system controlled by a volume receptor is more dominant than that controlled by an osmoreceptor. In 3 cases of inappropriate secretion of ADH, the mechanisms of ADH excess were examined. The first case had an adenocarcinoma of the lung, of which tissue extract showed no antidiuretic activity by bioassay. Autopsy revealed that the ADH excess might be caused by infiltration of the tumor into the left vagus nerve in the thoracic cavity. In the second case of a glioblastoma of the cerebellum, the cause of the syndrome was revealed to be destruction of the hypothalamo-neurohypophysial system by tumor infiltration and transient leak of ADH from the structure. The third case had an oat cell carcinoma of the lung. The ADH activity of the extract of the tumor was proved to be significantly high by both bioassay and radioimmunoassay. The results suggested an ectopic production of an antidiuretic substance closely similar to ADH (arginine vasopressin) in the tumor tissue.
Japan Society of Clinical Chemistryの論文

Control of Release of ADH and its Disturbance

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