Hypothalamic Somatostatin and LH-RH after Hypophysectomy, in Hyper- or Hypo-Thyroidism, and during Anesthesia in Rats

Abstract

Implants of growth hormone (GH) in the rat median eminence decrease pituitary weight and G H content, suggesting a negative feedback effect of G H at the hypothalamic level (1). Demonstration of the presence of TSH in the hypothalamus also implies that TSH might affect hypothalamic activity (2). Recently Oliver et al.(3) reported that hypophysial portal blood not only flows from median eminence to the pituitary gland but, as well, there is retrograde circulation via the neurohypophysis to the primary capillary plexus. Further, portal plasma contains high concentrations of both neurohypophysial and adenohypophysial hormones. These results favor a view that the pituitary hormones might exert a direct feedback control on the hypophysiotropic hormones of the hypothalamus. On the other hand, thyroidectomy results in the degranulation of the pituitary acidophil cells in rats (4), but also decreases pituitary G H content ( 5 ) , and impairs G H secretion (6). The mechanism by which T, and T3 influence G H synthesis in the pituitary is still unknown, but these thyroid hormones appear to exert a direct effect on the pituitary gland (7).Most anesthetics are known to change the rate of secretion of various pituitary hormones, probably by an effect mediated via the hypothalamus. The administration of sodium pentobarbital (Nembutal) into rats blocks the preovulatory surge of gonadotropin and ovulation (8). Nembutal increases serum G H and prolactin levels (9, lo), whereas urethane reduces G H and prolactin (1 1).Our recent studies using antiserum toThis study was supported in part by NIH research grants AM-09094 and AM-07467, and Veterans Administration.somatostatin indicated that this tetradecapeptide is involved in a regulatory mechanism of G H and TSH secretion in rats (12).The following questions could be raised: 1. If a short feedback regulatory mechanism takes place for G H and TSH secretion, does the removal of G H and TSH by hypophysectomy affect the hypothalamic somatostatin? 2. Does the absence or the excess of circulating thyroid hormone affect the hypothalamic somatostatin? 3. Do Nembutal and urethane modify somatostatin content of the hypothalamus? Our studies were designed to answer some of these questions.Materials and methods. Experimental procedures. Young adult male rats of CD strain from Charles River were used throughout the experiments. They were maintained at a constant temperature (24") and illumination (lights on 0500-1900 hr) and were given free access to tap water and Purina laboratory chow.In Exp. I, the rats were hypophysectomized when they were 35-days old and sacrificed by decapitation 24 days or 2.5 months after the operation. Intact agematched rats served as controls.In Exp. II,7O-day-old male rats, weighing 300-350 g, were divided into the following four groups: Group 1, intact control rats; Group 2, thyroidectomized rats. These two groups were injected with 0.2 ml of 0.9% saline subcutaneously (sc). Group 3, thyroidectomized rats were injected with 0.

Dichotomic action of glucocorticoids on growth hormone secretion

“…Wehrenberg et al (1983) reported an enhanced GH response to GHRH by Dex administration in vivo in rats. In view of the present study, this seems to be due to the pentobarbital anaesthesia, which is considered to be an inhibitor of SRIH release (Fernandez-Durango et al 1978), and, in their study, only the potentiating effect of Dex at the pituitary level would have been manifest.…”

“…However, several previous reports concerning the changes of the hypothalamic content of SRIH, decrease by hypophysectomy (Berelowitz et al 1981;Fernandez-Durango et al 1978;Wakabayashi et al 1976) or thyroidectomy (Berelowitz et al 1980) and increase by GH injection (Berelowitz et al 1981;Hoffman & Baker 1977), seem to indicate the parallel change of hypothalamic content and re¬ lease, at least in such subchronic or chronic states. Therefore, it can be presumed that the release of SRIH from the hypothalamus is increased in Dex-treated rats.…”

Immunoreactive Somatostatin in Rat Hypophysial Portal Blood*

“…The degradation of SRIF during the collection of hypophysial portal blood appears to be minimal, since no degradation of synthetic SRIF occurs in rat serum after 4 min at 37 C and 2 h at 0 C, i.e. It has been shown also that thyroidectomy and excess T 4 do not modify the hypothalamic SRIF (13) and TRH (14) contents. Although there is identical immunoreactivity between SRIF extracted from hypophysial portal plasma and synthetic SRIF, it cannot be concluded that SRIF in hypophysial portal blood is identical to synthetic SRIF.…”

Thyroidectomy Abolishes Pulsatile Growth Hormone Secretion without Affecting Hypothalamic Somatostatin

“…In the latter case, they could eitherstimulate SRIF or inhibit GRF release, or modulate other neuropeptides such as TRH which interfere with GH secretion [27], In our experimental conditions neither SRIF content nor release from the hypo thalamus were affected 5 weeks after thyroidectomy, a find ing consistent with that of Fernandez-Durango z t al. [13]. A primary effect of thyroid hormones on SRIF synthesis and/ or release thus appears unlikely to account for their action on GH secretion, as further suggested by the ineffectiveness of thyroidectomy and thyroxine to modify SRIF levels in the hypophyseal blood [14].…”