Effects of α- and β-Adrenergic Inhibition and Somatostatin on Plasma Glucose, Free Fatty Acids, Insulin, Glucagon, and Growth Hormone Responses to Prostaglandin E1in Man*

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Abstract
It has been previously shown that prostaglandin E1 (PGE1) induced a significant increase in plasma glucose, FFA, glucagon, and GH levels when infused in normal man. In the present study, we evaluated the effects of α- and β-adrenergic blockers and somatostatin on these metabolic and hormonal responses to PGE1. The pretreatment with propranolol (0.08 mg/min) reduced basal plasma glucagon from a mean value of 86 ± 6 to 70 ± 8 pg/ml (mean ± SEM; P < 0.05) and completely blunted glucagon and FFA responses to PGE1 (0.2 μg/kg-min), but did not interfere with the rise in plasma glucose or GH levels. Phentolamine pretreatment (0.5 mg/min) caused a significant increase in basal glucagon and insulin (P < 0.05). Phentolamine had no effect on the responses of the various parameters to PGE1. Plasma insulin levels remained essentially unchanged during the development of hyperglycemia during both α and β blockade. Somatostatin (250 μg/h) lowered basal plasma insulin and glucagon (P < 0.01) and prevented glucagon and GH increases by PGE1. By contrast, plasma glucose rose from a mean basal value of 85 ± 4 to 135 ± 7 mg/100 ml (P < 0.001), and plasma FFA rose from a prestimulatory value of 600 ± 70 to 775 ± 76 μeq/liter (P < 0.05) after PGE1. Plasma glucose and FFA levels were significantly higher during PGE1 and somatostatin administration than when PGE1 was given alone. These results suggest that some (glucagon and FFA) but not all (glucose and GH) responses to PGE1 are mediated by the β-adrenergic system, that PGE1 inhibits insulin secretion not mediated by α stimulation, and that somatostatin blocks the increases in glucagon and GH resulting from PGE1 and also potentiates its hyperglycemic and lipolytic effects.