Abstract
To evaluate the GH regulating mechanism in acromegalic patients, postinhibitory 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 (500μg/75min) 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 45min in normal controls and at 75min in acromegalic patients after the cessation of somatostatin infusion. Dopamine (DA) infusion (5μg/kg/min for 90min) 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%·min vs 3682.5±295.5%·min) during the DA or somatostatin infusion were not different, the rebound at 15min was significantly greater after DA than after somatostatin (p<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. These results indicate that the mechanism participating in the postinhibitory rebound rise is different between normal controls and acromegalic patients, and the rebound rises induced by somatostatin and DA might occur through the different mechanisms. Also, it is evident that the rebound phenomenon in acromegaly is possibly modified by endogenous hypothalamic releasing factors.
