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The metabolic effects of dopamine in man
Abstract:
The metabolic effects of dopamine have been investigated by its infusion in normal man with and without simultaneous somatostatin administration. Dopamine was infused into overnight fasted men at 1.5 microgram/kg/min (n = 6) and 3.0 micrograms/kg/min (n = 5) for 120 min. Plasma dopamine concentrations at 120 min were 78 +/- 9 nmol/l and 117 +/- 17 nmol/l respectively, associated with a marginal rise in plasma noradrenaline. Dopamine (1.5 microgram/kg/min) induced an early and sustained rise in plasma glucagon (48 +/- 9 pg/ml versus 19 +/- 6 pg/ml in saline controls at 10 min, p less than 0.01) and a transient elevation in serum growth hormone which peaked to 17.7 (range 4.5-71.8) mU/l at 60 min (7.2 (range 0.6-37.7) mU/l with saline, p less than 0.05) but did not alter serum insulin, blood glucose or other metabolite levels. At 3.0 micrograms/kg/min, dopamine in addition provoked mild and transient elevations in blood glucose and serum insulin. Somatostatin (250 micrograms/h) suppressed circulating insulin, glucagon, and growth hormone levels and abolished the small hyperglycaemic effect seen with the higher dopamine dose. Somatostatin alone induced a progressive rise in circulating non-esterified fatty acid and 3-hydroxybutyrate levels reflecting insulin deficiency. This rise in NEFA and 3-hydroxybutyrate was increased by dopamine particularly at the higher dosage (plasma NEFA; somatostatin alone, 1.08 +/- 0.13 mmol/l; somatostatin plus dopamine 3 micrograms/kg/min, 1.44 +/- 0.17 mmol/l at 120 min, p less than 0.01: blood 3-hydroxybutyrate; somatostatin alone, 0.32 +/- 0.04 mmol/l; somatostatin plus dopamine 3 micrograms/kg/min, 0.56 +/- 0.12 mmol/l at 120 min, p less than 0.05). Thus: 1) dopamine at pharmacological dosage has minor effects when other endocrine mechanisms are intact, 2) it enhances lipolysis and ketogenesis during somatostatin-induced insulin deficiency; 3) the hyperglycaemia effect of the higher dopamine dose is probably mediated through stimulated glucagon secretion.