Modulation of postinhibitory rebound rise in plasma GH by hypothalamic hormones in patients with acromegaly.

Abstract

To evaluate the GH regulating mechanism in acromegalic patients, post-inhibitory rebound rise in GH secretion induced by somatostatin was studied in these cases and normal subjects, and was compared with the rebound GH rise induced by dopamine. After somatostatin infusion (500 micrograms/75 min) both 5 normal and 9 acromegalic subjects showed prompt GH decreases during the infusion (% decrease: 69.1 +/- 10.4 vs 74.4 +/- 5.1) and showed rebound rises after its termination. However, the rebound rises occurred more promptly and markedly in normal controls than in acromegalic patients, i.e. the rebound peak appeared at 45 min in normal controls and at 75 min in acromegalic patients after the cessation of somatostatin infusion. Dopamine (DA) infusion (5 micrograms/kg/min for 90 min) also induced similar inhibition and postinhibitory rebound rises in GH secretion in 7 patients with acromegaly. Although the maximum inhibition (65.6 +/- 6.4% vs 74.4 +/- 5.1%) and the inhibitory area (4338.0 +/- 481.5% X min vs 3682.5 +/- 295.5% X min) during the DA or somatostatin infusion were not different, the rebound at 15 min was significantly greater after DA than after somatostatin (p less than 0.02). When TRH was injected at the termination of somatostatin infusion, the rebound increase was significantly enhanced and the rebound peak appeared 45 min earlier than after a single somatostatin administration. Similarly, hp GRF (1-44)-NH2 enhanced the postinhibitory rebound rises in 4 patients studied.(ABSTRACT TRUNCATED AT 250 WORDS)