Hyperglucagonemia and alpha-adrenergic receptor in acute hypoxia.
The plasma immunoreactive glucagon (IRG) response to hypoxia was studied in puppies. Three groups of paired experiments were performed. In group I, 8% O2:92% N2 ventilation (PaO2 20--30 torr) produced a rise in plasma IRG and glucose as well as hypotension and bradycardia. However, when group I was air ventilated (PaO2 greater than 70 torr) and given glucose infusions producing hyperglycemia of similar degree, plasma IRG was unchanged. Group II received alpha-adrenergic blockade (phenoxybenzamine). When made hypoxic, group II developed no significant IRG rise and less hyperglycemia than with hypoxia alone. Hypotension was more severe with hypoxia plus alpha-blockade. Phenoxybenzamine itself did not change plasma IRG or glucose during air breathing. Group III receivi developed hyperglucagonemia and hyperglycemia not significantly different from that with hypoxia alone. However, hypoxia-caused hypotension and bradycardia was more pronounced with beta-blockade. No change in plasma IRG or glucose occurred in group III animals breathing air. These data suggest that a) glucagon release is caused by acute oxygen deficiency, and b) the hypoxic response is largely adrenergically mediated with the major role played by the alpha-receptor.
D000818:Animals; D001786:Blood Glucose; D001794:Blood Pressure; D004285:Dogs; D005934:Glucagon / Q000097:blood*; D006339:Heart Rate; D000860:Hypoxia / Q000097:blood*; D010643:Phenoxybenzamine / Q000494:pharmacology; D011433:Propranolol / Q000494:pharmacology; D011941:Receptors, Adrenergic / Q000502:physiology*; D011942:Receptors, Adrenergic, alpha / Q000502:physiology*
D001786:Blood Glucose; D011941:Receptors, Adrenergic; D011942:Receptors, Adrenergic, alpha; D010643:Phenoxybenzamine; D005934:Glucagon; D011433:Propranolol