Critical comments on the classic concept of hypoglycemia induced epinephrine secretion.
Our experiments showed that a continuous chronic administration of norepinephrine (NE) to rats for 20 h by means of subcutaneously implantable retard tablets, led to a highly significant epinephrine(E) depletion of the adrenal medulla during normoglycemia. The rise of free plasma NE was accompanied by increased free plasma E values at 12 hours. At this time the liver contents of glycogen and free intracellular glucose showed their most pronounced decrease. At 12 and 20 hours both liver glycogen and medullar E values were very low. To check a possible causal relationship between those two events another experiment was performed in which the breakdown of liver glycogen should be inhibited. NE treated rats were force fed with 50% glucose solution 9 h after tablet implantation. This resulted in only mild glycogen depletion, which was no more able to trigger E liberation from the medulla. Therefore we conclude that pronounced liver glycogen depletion possesses a triggering ability for medullar E output by which hypoglycemia could be prevented.
Porta
S
S
Institute of Functional Pathology, Clinical and Experimental Endocrinological Research Unit, University of Graz, Austria.
Emsenhuber
W
W
Supanz
S
S
Korsatko
B
B
D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D004343:Drug Implants; D004837:Epinephrine / Q000097:blood*; D007003:Hypoglycemia / Q000097:blood*; D008099:Liver / Q000378:metabolism; D009638:Norepinephrine / Q000097:blood / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains
D001786:Blood Glucose; D004343:Drug Implants; D009638:Norepinephrine; D004837:Epinephrine