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Abstract
The effects of the non-peptide vasopressin V2 receptor antagonist, 5-dimethylamino-1-[4-(2-methylbenzoylamino)benzoyl]-2,3,4,5-tetrah
ydro-1 H-benzazepine hydrochloride (OPC-31260) on the cerebral oedema induced by subarachnoid
haemorrhage were studied in rats. Subarachnoid haemorrhage induced significant water
retention after water loading, increased the brain content of water and Na+ and increased
plasma vasopressin levels. The water retention and brain water and Na+ accumulation
were prevented by OPC-31260 administration, but the plasma vasopressin levels were
further enhanced by OPC-31260. These results demonstrate the important role of vasopressin
in the development of antidiuresis and disturbances in brain water and electrolyte
balance in response to subarachnoid haemorrhage. The subarachnoid haemorrhage-induced
cerebral oedema was significantly reduced following oral OPC-31260 administration.
The protective mechanism exerted by OPC-31260 stems from its influence on renal tubular
function: it blocks the renal vasopressin V2 receptors. These observations might suggest
a new, effective approach to the treatment of subarachnoid haemorrhage-induced cerebral
oedema in humans.