In vivo evidence of a positive role for somatostatin to optimize pulsatile growth hormone secretion. Turner, Joel P., and Gloria Shaffer Tannenbaum. Departments of Pediatrics, Neurology and Neurosurgery, McGill University; and the Neuropeptide Physiology Laboratory, McGill University-Montreal Children's Hospital Research Institute, Montreal, Quebec H3H 1P3, Canada.
APStracts 2:0097E, 1995.
Despite convincing evidence that somatostatin (SRIF) and GH-releasing factor (GRF), individually, play crucial roles in GH regulation, the nature of the interplay between these two hypothalamic hormones is far from clear. In the present study, we used the long-acting SRIF analog, octreotide, as a probe in both the normal and mutant dwarf (dw) rat, to 1) further elucidate the temporal nature of the SRIF/GRF interaction in vivo and 2) define possible mechanisms of action of SRIF in generating pulsatile GH secretion. Normal free-moving adult male rats pretreated with octreotide (25 and 50 [mu]g iv) and subsequently challenged with GRF (1 [mu]g iv) exhibited a markedly blunted GH response to exogenous GRF 1 h after treatment. In contrast, preexposure to octreotide for 3 h produced a 2- to 3-fold augmentation in GH responsiveness to GRF. When compared to normal saline-pretreated controls, 3 h pretreatment with octreotide produced a 14- to 16-fold augmentation in the postinhibitory rebound release of GH following the co-administration of native SRIF-14 and GRF (P<0.001). In dw rats, which show a selective reduction in GH synthesis and storage, 3 h preexposure to octreotide failed to significantly alter GRF-induced GH release. These results demonstrate that, in the normal male rat, a 3-h period of exposure to the SRIF analog, octreotide, is sufficient to enhance GH responsiveness to GRF. Our findings suggest that this effect is due to a SRIF-mediated build-up of pituitary GH stores in a readily releasable pool. We conclude that SRIF is not only inhibitory to GH but has an important positive role to play in the generation of GH pulses by preparing the somatotroph to respond optimally to the next pulse of hypothalamic GRF. 

Received 28 February 1995; accepted in final form 26 April 1995.
APS Manuscript Number E94-5.
Article publication pending Am. J. Physiol. (Endocrinol. Metab.).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on  9 May 1995.