Hypoglycemia induced by alpha-adrenergic stimulation during alkalosis.
Hypoglycemia developed during respiratory alkalosis in fasted rats. This hypoglycemia was markedly potentiated by the simultaneous injection of inhibitors of hepatic gluconeogenesis or a beta-adrenergic blocking agent; was not influenced by anti-insulin serum; was attenuated by hexamethonium; and was abolished by an alpha-adrenergic blocking agent. The rate of removal of injected glucose by peripheral tissues increased during alkalosis in insulin-deficient rats. The uptake of [14C]-glucose by the adipose tissue in vivo, which is stimulated by a very minute amount of insulin, was also stimulated during alkalosis whether or not the circulating insulin was neutralized with anti-insulin serum. It was concluded that, in alkalotic rats, blood glucose is rapidly utilized by peripheral tissues dependent on alpha-adrenergic stimulation, but without mediation of insulin and that this leads to development of hypoglycemia.
D000472:Alkalosis, Respiratory / Q000150:complications* / Q000378:metabolism / Q000503:physiopathology; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism*; D005230:Fatty Acids, Nonesterified / Q000097:blood; D005943:Gluconeogenesis / Q000187:drug effects; D005947:Glucose / Q000378:metabolism; D007003:Hypoglycemia / Q000097:blood / Q000209:etiology*; D007328:Insulin / Q000097:blood / Q000494:pharmacology; D008297:Male; D051381:Rats; D011941:Receptors, Adrenergic / Q000502:physiology*; D011942:Receptors, Adrenergic, alpha / Q000187:drug effects / Q000502:physiology*; D013268:Stimulation, Chemical; D013997:Time Factors
D001786:Blood Glucose; D005230:Fatty Acids, Nonesterified; D007328:Insulin; D011941:Receptors, Adrenergic; D011942:Receptors, Adrenergic, alpha; D005947:Glucose