Why the study?
Does intracerebroventricular administration of the somatostatin analog ODT8-SS suppress the rise in plasma catecholamines induced by neural stimuli?
Does intracerebroventricular administration of the somatostatin analog ODT8-SS suppress the rise in plasma catecholamines induced by neural stimuli?
The somatostatin analog ODT8-SS acts within the central nervous system to modulate sympathetic nervous system activity by suppressing stimulus-induced rises in plasma catecholamines.
Central ODT8-SS effects on sympathetic activity in animals leave open translation to human cardiovascular therapies.
The somatostatin analog, des-AA1,2,4,5,12,13-[D-Trp8]somatostatin (ODT8-SS), acts within the central nervous system to suppress the rise in plasma catecholamines associated with a variety of neural stimuli. Insulin-induced hypoglycemia or stress caused significant elevations in plasma catecholamines that were abolished by intracerebroventricular (icv) administration of ODT8-SS. Bombesin, carbachol, or 2-deoxyglucose, injected icv, evoked marked elevations in plasma epinephrine and norepineprine. These effects were also prevented by ODT8-SS given icv. In all experiments, ODT8-SS appeared to be more effective in lowering plasma epinephrine than in lowering plasma norepinephrine. Systemic administration of ODT8-SS was ineffective in lowering plasma catecholamine levels. Native somatostatin given icv produced inconsistent effects on plasma catecholamine levels. These data suggest that the somatostatin analog, ODT8-SS, acts within the central nervous system to modulate sympathetic nervous system activity. It is suggested, but not established, that this analog acts through the same receptor as native somatostatin.
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Fisher et al. (1980) studied this question.
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