Role of somatostatin in the modulation of hypophysial growth hormone production by gonadal steroids

Abstract

Growth hormone-release-inhibiting hormone (somatostatin) has been localized in several central nervous system sites, but the contribution of somatostatin in these various loci to the control of growth hormone (GH) production is unclear. In the present study, the efficacy of castration, alone, or with subsequent gonadal steroid administration, in modulating hypophysial GH production was examined, and the response of somatostatin-containing nerve endings in the median eminence and the organum vasculosum of the lamina terminalis (OVLT) was evaluated by means of immunocytochemistry. Orchidectomy reduced the size and number of immunoreactive GH-cells, and testosterone administration prevented this change. Ovariectomy appeared to stimulate the somatotropes, but this effect was neither as dramatic nor as consistent as the effect of castration in the male. Administration of estradiol, however, resulted in a marked reduction in the number, size, and GH content of somatotropes in all animals examined. Somatostatin was localized in the ext.erne1 lamina of the median eminence and in nerve endings surrounding the core of capillaries in the OVLT. Only the median eminence responded to steroid manipulations with a visible change in the immunoreactive pool of somatostatin, with a decrease following orchidectomy, which was reversible by testosterone treatment, and an increase following ovariectomy, which was reversible by estradiol treatment. However, as in the GH responses to steroid manipulations, the somatostatin responses were more variable in females than in males.These results suggest that: 1) testosterone promotes and estradiol, a t least at high doses, inhibits storage of GH in the anterior pituitary; 2 ) these changes in GH production may be regulated, in part, by altered somatostatin release from the median eminence into the hypophysial portal blood; and 3) somatostatin in the OVLT may not be involved in the steroid-induced modulation of GH production.Currently available evidence supports the hypothesis that a dual neural regulation of growth hormone (GH) secretion exists. The predominant control is believed to be stimulatory, mediated by a growth hormone-releasing factor (Martin, '76). Although the existence of this releasing factor is supported by considerable experimental evidence, its isolation and characterization have not been achieved; thus, specific techniques for its localization and measurement can not yet be applied. The inhibitory control is thought to be mediated by growth hormone-release-inhibiting hormone, or somatostatin, which has been isolated, char. acterized, and synthesized (Brazeau et al., '73). Using both radioimmunoassay (Brownstein e t al., '75; Epelbaum e t al., '77; Kobayashi et al., '77; Pate1 and Reichlin, '78) and immunocytochemistry (see Zimmerman, '77; Elde e t al., '78 for reviews), somatostatin has been localized in several central nervous system sites, including both hypothalamic and extrahypothalamic areas. There appear to be several general patterns of somatostatin localizatio...

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