We studied the contribution of α- and β-adrenergic receptor activation to the cardiovascular, metabolic, and hormonal effects of dopamine. At a concentration of 1.5 μg/kg·min, the infusion of dopamine in 12 normal volunteers was associated with a transient but significant rise in pulse rate, which was prevented by propranolol. Venous plasma glucose did not change throughout the experiments, and a mild increase in plasma free fatty acid levels observed during the administration of dopamine alone was antagonized by propranolol. In contrast, neither the β-adrenergic blocker, propranolol, nor the α-adrenergic blocker, phentolamine, was effective in inhibiting the dopamine-induced rise in plasma glucagon (from 82±9 to 128±14 pg/ml; P < 0.005) and serum insulin (from 7.5±1 to 13±1.5 μU/ml; P < 0.005) or its suppression of plasma prolactin (from 8.5±1 to 5.2±0.8 ng/ml; P < 0.001). Although serum growth hormone levels did not change during the infusion of dopamine alone, an obvious rise occurred in three subjects during the combined infusion of propranolol and dopamine.
Mara Lorenzi, John H. Karam, Eva Tsalikian, Nancy V. Bohannon, John E. Gerich, Peter H. Forsham
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