Autonomic Neural Control Mechanisms and the Release of Adrenal Steroids after Hypoglycaemia in Man

Summary

The changes in blood glucose, plasma potassium, plasma renin activity, aldosterone, cortisol, corticosterone and ACTH were measured in 11 normal subjects, 6 tetraplegic subjects (pre-ganglionic sympathectomy) and 6 tetraplegic subjects given atropine (sympathectomy with cholinergic blockade), in response to acute insulin-induced hypoglycaemia. After hypoglycaemia, blood glucose recovery was impaired only in the tetraplegic group given atropine in whom ACTH secretion was delayed and the peak cortisol and corticosterone concentrations were lower compared with the other groups. Plasma renin activity rose both in the normal and the tetraplegic subjects; the aldosterone rise and the fall in potassium were similar in all three groups. Aldosterone release after hypoglycaemia appears to occur independently of stimulation of the sympatho-adrenal system and cholinergic blockade, and may result from activation of the renin-angiotensin system, rather than from ACTH stimulation. Activation of ACTH secretion in response to hypoglycaemia may involve a cholinergic mechanism at the hypothalamic level, with a consequent reduction in the increments of plasma cortisol and corticosterone after atropine administration.

Key-Words:

Hypoglycaemia - Tetraplegia - Plasma Renin Activity - Adrenal Steroids - ACTH - Aldosterone