Effects of somatostatin and hypothalamic ventromedial lesions on GH release induced by morphine

Morphine in intravenous doses ranging from 10 mug/kg to 8 mg/kg was shown to be effective in stimulating GH release in the unanesthetized rat. The response to the log of the dose was linear over a range of 10 to 1000 mug/kg. Somatostatin (GH-release inhibiting factor) administered SC in a dose of 200 mug/kg 5 min before morphine prevented the GH rise. Neither inhibitors of catecholamine or serotonin synthesis nor blockage of alpha and beta-adrenergic receptors had any effect on the response. The response was partially blocked in animals with large hypothalamic ventromedial (VMN) lesions. Such lesions completely abolished the GH response to pentobarbital. These results indicate that morphine is a remarkably potent agent for stimulation of GH release but the precise mechanism and site of action of the drug remain to be determined.