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

The spectrum of GH responses to GHRH and somatostatin in patients with acromegaly.

“…Although, the exact reason for the difference between the group I and group II is not clear, it is plausible that the receptor and post receptor system in group II somatotrophs are less operative than in group I. The fact that in group I (• •, n=32) and group II the postinhibitory GH rise after somatostatin infusion was much smaller in group II than in group I suggests the following possibilities, 1) intracellularly stored GH pool was smaller in these patients due to lesser GH inhibition, 2) negative feedback effects on their hypothalamic GHRH or somatostatin were less prominent, or 3) these somatotrophs were less responsive to endogenous hypothalamic stimulations through such feedback (Hanew et al 1984). From the data of similar plasma TSH responses to TRH in the two groups, it seems that negative feedback effects of OH on hypothalamic somatostatin secretion are essentially not different in the two groups, since it is well known that somatostatin can regulate TSH secretion in man and rat (Siler et al 1974;Chihara et al 1978 (Shibasaki et al 1986).…”

Modulation of postinhibitory increase in plasma prolactin by domperidone in patients with prolactin secreting adenoma.

“…Usually, pituitary hormones show rebound rises exceeding the basal levels after the administration of inhibitory agents (Hall et al, 1973;Leblank et al, 1976;Leebaw et al, 1978;Kaptein et al, 1980;Hanew et al, 1984). The postinhibitory rebound rises are considered to be a mechanism for maintaining the homeostatic hormone secretion.…”