Sodium Salicylate Augments the Plasma Adrenocorticotropin and Cortisol Responses to Insulin Hypoglycemia in Man*

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Abstract
To test the hypothesis that prostaglandins attenuate neuroendocrine responses to changes in circulating glucose levels in man, we studied the effects of sodium salicylate (SS), a prostaglandin synthesis inhibitor, on the plasma ACTH and cortisol responses to insulin hypoglycemia. Six normal men were given insulin (0.05 U/kg, iv) on 2 different days during the infusion of either SS (40 mg/min) or saline. Compared to the saline control, SS had no significant effect on either the rate of fall of plasma glucose after insulin or the glucose nadir (mean ± SEM, 33 ± 3 us. 36 ± 3 mg/dl; P = NS). Peak ACTH levels after insulin were higher during SS compared to those during saline in all six subjects (316 ± 95 vs. 102 ± 26 pg/ml; P < 0.05), and SS had a clear effect to increase both the overall ACTH response (F = 21.3; P < 0.01, by analysis of variance) and the plasma cortisol response (F= 6.72; P < 0.05, by analysis of variance). The most striking example of this effect of SS occurred in one subject whose peak plasma ACTH was only 44 pg/ml during saline but reached 750 pg/ml during SS despite an identical fall of plasma glucose to 42 mg/dl. Augmentation of the ACTH and cortisol responses to insulin hypoglycemia may be the result of an alteration by SS of recognition of glucose levels by glucose-sensitive cells of the brain, an effect which could be due to the inhibition of prostaglandin synthesis.