The role of the beta-adrenergic mechanism in the hypergastrinemia of hyperthyroidism.

Abstract

To investigate the role of the β-adrenergic mechanism in the hypergastrinemia of hyperthyroidism, either a β-adrenergic blocking agent or a β-adrenergic stimulating agentwas administered to patients with hyperthyroidism, to patients with atrophic gastritis, and to normal subjects. Compared to normals, fasting plasma levels of gastrin were elevated in patients with hyperthyroidism and atrophic gastritis [87 ± 4 us. 306 ± 45 or 249 ± 37 pg/ml (mean ± SE); P < 0.01]. After propranolol infusion (20 mg over 60 min), plasma gastrin levels significantlydecreased in hyperthyroid patients to 147 ± 25 pg/ml (P < 0.01). Similarly, in patients with atrophic gastritis and in normal subjects, propranolol infusion was accompanied by a decrease in plasma gastrin levels to 195 ± 34 and 70 ± 5 pg/ml, respectively(P < 0.05). However, the mean maximum percent decrement of plasma gastrin from the basal levels was 2- to 3-fold greater in hyperthyroid patients than in patients with atrophic gastritis or in normal subjects (P < 0.01). Isoproterenol infusion (30 /ng over 20 min) elicited a rise in plasma gastrin in both normal subjects and patients with hyperthyroidism and atrophic gastritis. The mean maximum percent increment of plasma gastrin in hyperthyroid patients was significantly greater than that in normal subjects or in patients with atrophic gastritis (185 ± 18% vs. 128 ± 11% or 137 ± 10% P < 0.05). These results suggest that hypersensitivity of the β-adrenergic mechanism is responsible for the elevated gastrin levels in hyperthyroidism but not in patients with atrophic gastritis.