Endogenous Catecholamines Modulate Growth Hormone Release in the Conscious Rat During Hypoglycaemia but not in the Basal State

To investigate the role of endogenous catecholamines and 5‐hydroxytryptamine in the control of growth hormone (GH) secretion, secretory profiles of GH and prolactin were measured in conscious, male rats following intravenous administration of either 1) α₂ antagonist idazoxan 2 mg/kg, a dose that blocked α₂ agonist induced GH rise, 2) α₁ antagonist prazosin 1 mg/kg, 3) non‐specific β‐blocker propranolol 1.5 mg/kg, a dose that prevented β₂ agonist (salbutamol) induced inhibition, 4) serotonin antagonist cyprohep‐tadine 0.5 mg/kg, a dose that inhibited serotonin agonist quipazine induced GH rise, or 5) control. No drug altered mean GH or prolactin levels and pulsatile GH release persisted. Unilateral injections of prazosin, propranolol and idazoxan were made into the medial basal hypothalamus and preoptic‐anterior hypothalamic area and of cyproheptadine into the medial basal hypothalamus, all with no effect on short‐term GH release. GH and prolactin secretory profiles were measured after giving rats 6 units/kg intravenous insulin. Blood glucose levels fell to less than 50% basal. Hypoglycaemia caused a non‐significant 30% fall in mean 2 h GH. Intravenous idazoxan, prazosin, propranolol and cyproheptadine (doses as in first study) did not modify the blood glucose fall, but idazoxan produced a significant reduction of mean GH compared to insulin alone (4 ± 1.1 ng/ml SEM, idazoxan/insulin versus 16 ± 5.6 ng/ml, saline/insulin). The lack of an effect of a‐ and β‐blockers on normal, pulsatile GH release is against a role for endogenous catecholamines in controlling this release. Catecholamines may be released during insulin‐induced hypoglycaemia and preferentially bind to α₂ receptors to increase GH secretion, thus attenuating the suppression of GH levels that would otherwise occur.