Acute cellular glucopenia after 2-deoxy-D-glucose administration profoundly stimulates hypothalamic-pituitary-adrenocortical and adrenomedullary activity. Whether glucopenia stimulates sympathoneural release of noradrenaline is unclear. We studied 20 healthy subjects who received 2-deoxy-D-glucose (50 mg/kg in 100 ml isotonic saline) or isotonic saline (100 ml) i.v. for 30 min on each of 2 test days. Heart rate and blood pressure were measured with antecubital venous blood obtained via an indwelling catheter for assays of plasma catecholamines (noradrenaline; adrenaline; dihydroxyphenylalanine; dihydroxyphenylglycol; and dihydroxyphenylacetic acid), corticotrophin, cortisol, and glucose. 2-deoxy-D-glucose decreased diastolic blood pressure by 20% (from 69 ± 2 to 55 ± 2 mmHg) and increased adrenaline levels by 30-fold [21 ± 6 (SEM) to 634 ± 73 pg/ml], corticotrophin by seven-fold (5.1 ± 1.2 to 35.8 ± 4.9 pg/ml), glucose and cortisol by two-fold (82 ± 5 to 163 ± 9 mg/dl and 15 ± 2 to 31 ± 2 μg/dl), and noradrenaline by about 30% (224 ± 15 to 295 ± 24 pg/ml, p < 0.05), whereas plasma dihydroxy-phenylglycol levels decreased (765 ± 56 to 628 ± 42 pg/ml). Small decreases in dihydroxyphenylalanine and dihydroxyphenylacetic acid levels after 2-deoxy-D-glucose did not differ from those after saline. Responses of adrenaline levels were positively correlated with those of noradrenaline (r = 0.47, p < 0.05) and glucose (r = 0.45, p = 0.06), but not of corticotrophin. We conclude that acute glucopenia evoked by 2-deoxy-D-glucose markedly activates the hypothalamic-pituitary-adrenocortical and adrenomedullary systems concurrently in man, without evidence for increases in exocytotic release, turnover, or overall synthesis of noradrenaline in sympathetic nerves. Increments in noradrenaline levels in this setting seem to be due mainly to a marked increase in adrenomedullary secretion, which probably also determines the hyperglycaemic reponse.
- Dihydroxyphenylacetic acid
- Sympathetic nervous system
ASJC Scopus subject areas
- Endocrine and Autonomic Systems
- Clinical Neurology