AJP - Endocrinology and Metabolism, Vol 256, Issue 2 E231-E235, Copyright © 1989 by American Physiological Society
Hypothalamic noradrenergic and sympathoadrenal control of glycemia after stress
G. A. Smythe, W. S. Pascoe and L. H. Storlien
Garvan Institute of Medical Research, St. Vincent's Hospital, Darlinghurst, New South Wales, Australia.
Central noradrenergic pathways play a significant role in mediating blood
glucose levels after neuroglycopenia. To further investigate hypothalamic
noradrenergic neuronal activity (NNA) and sympathoadrenal influences in
glucoregulation, we studied the effects of acute stress on glycemia and
insulin release in normal and adrenalectomized (ADRX) rats. Within 5 min of
exposure of rats to ether or cold-swim stress, significant positive
correlations were evident between hypothalamic NNA and serum glucose levels
(r = 0.70, P less than 0.001; at 15 min r = 0.78, P less than 0.0001). Five
minutes after stress in the intact rat, insulin release was inhibited and
serum insulin levels inversely correlated to hypothalamic NNA (r = 0.45, P
less than 0.05). This relationship between insulin and NNA was no longer
present 15 min after stress, but the levels of insulin remained
inappropriately low with respect to the elevated serum glucose levels
(approximately 30% above basal). Blockade of sympathetic noradrenergic
pathways by treatment of intact rats with guanethidine prevented the rise
in glucose after cold-swim stress but did not prevent the inhibition of
insulin release. Fifteen minutes after exposure of ADRX rats to cold-swim
stress their hypothalamic NNA and serum glucose levels were similar to
intact animals. However, in contrast to their intact counterparts, serum
insulin levels were significantly elevated (P less than 0.01). These data
are consistent with central noradrenergic neural pathways directly
mediating hepatic glucose release and indirectly inhibiting pancreatic
insulin release via activation of adrenal medullary catecholamines.
