Plasma levels of catecholamines and corticotrophin during acute glucopenia induced by 2-deoxy-D-glucose in normal man

Abstract

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)

Sympathoneural and Adrenomedullary Responses to Mental Stress

“…It is very difficult to evaluate catecholamine reactivity to mental stress in a manner that (1) is independent of physical activity, which would be expected to increase sympathetic noradrenergic outflows and plasma NE levels differentially with respect to sympathetic adrenergic outflows and plasma EPI levels [133, 134]; (2) involves real-life distress, as opposed to laboratory challenges that are not particularly distressing [104]; (3) includes baseline measures prior to the stress [40]; and (4) takes into account factors such as systemic hemodynamics [135], posture [136], room temperature [137], meal ingestion [138, 139], the state of glycemia [140, 141], which differentially affects sympathetic adrenergic outflow, and medications [142, 143]. With these limitations in mind, the following discussion highlights particular areas in which catecholamine reactivity to mental stress may play a role in the pathogenesis of a variety of disorders.…”

Plasma catecholamines and blood volume in native Andeans during hypoxia and normoxia

“…For instance, exposure to cold preferentially stimulates sympathoneural outflows [10], whereas hypoglycemia preferentially stimulates adrenomedullary secretion [12]. The role of locally produced dopamine in chronic adaptive responses to hypoxia remains poorly understood.…”

Effects of pharmacological doses of 2-deoxyglucose on plasma catecholamines and glucose levels in patients with schizophrenia

“…Assuming that plasma clearance of NE was not decreased during the 2DG glucoprivation, the increments of NE must have been secondary to an increase in spillover, which is determined by the rate of release from the sympathetic nerves, the adrenal medulla or a combination of both. Studies of 2DG in healthy volunteers have attributed the 2DG-induced NE elevations mainly to the adrenomedullary rather than sympathoneural secretion since these NE elevations were associated with no concurrent increases in DHPG (actually, significant decreases were reported ;Breier 1989;Goldstein et al 1992;Breier et al 1992). This is because sympathoneural (but not adrenomedullary) stimulation concurrently increases plasma NE and DHPG levels due to increased reuptake of the released NE (Goldstein 1995).…”

“…Additionally, insulin may hamper the distinction of primary homeostatic dysregulation from group differences in response to aversive physiological and psychological factors since it exaggerates sympathetic autonomic responses (Davis et al 1993a,b) leading to marked anxiety and physical distress (Goldstein 1995).…”