Goldstein D S, Breier A, Wolkowitz O M, Pickar D, Lenders J W
Clinical Neuroscience Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD.
Clin Auton Res. 1992 Dec;2(6):359-66. doi: 10.1007/BF01831392.
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 sevenfold (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 micrograms/dl), and noradrenaline by about 30% (224 +/- 15 to 295 +/- 24 pg/ml, p < 0.05), whereas plasma dihydroxyphenylglycol 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.(ABSTRACT TRUNCATED AT 250 WORDS)
