1990
DOI: 10.1159/000125322
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Effects of Intracerebroventricular Administration of Growth Hormone-Releasing Factor and Corticotropin-Releasing Factor on Somatostatin Secretion into Rat Hypophysial Portal Blood

Abstract: To clarify the regulatory mechanisms for the secretion of somatostatin (SRIF) from the hypothalamus, the effects of intracerebroventricular (i.c.v.) administration of growth hormone-releasing factor (GRF) and corticotropin-releasing factor (CRF) on SRIF secretion into hypophysial portal blood were examined in pentobarbital-anesthetized male rats. Neither the concentration of SRIF in portal plasma nor the secretion rate of SRIF was changed after i.c.v. administration of 0.9% saline. Administration of 10 ng or 5… Show more

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Cited by 51 publications
(35 citation statements)
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“…Injections of somatostatin or its analogues into the third ventricle of rats inhibit stress-induced ACTH secretion by attenuating endogenous CRH release (Brown et al, 1984). On the other hand, a stimulatory effect of CRH on somatostatin release in vitro and in vivo have also been demonstrated (Mitsugi et al, 1990). Taken together, these results show close interactions between CRH and somatostatin secretory neurons and thereby somatostatin seems to be a hypothalamic hormone strongly involved in stress responses.…”
Section: Invited Full-reviewmentioning
confidence: 69%
“…Injections of somatostatin or its analogues into the third ventricle of rats inhibit stress-induced ACTH secretion by attenuating endogenous CRH release (Brown et al, 1984). On the other hand, a stimulatory effect of CRH on somatostatin release in vitro and in vivo have also been demonstrated (Mitsugi et al, 1990). Taken together, these results show close interactions between CRH and somatostatin secretory neurons and thereby somatostatin seems to be a hypothalamic hormone strongly involved in stress responses.…”
Section: Invited Full-reviewmentioning
confidence: 69%
“…However, the purely systemic-central nervous system (CNS) feedback structure fails to account for other fundamental experimental observations. The latter include 1) continued GH pulsatility under constant systemic GHRH stimulation, 2) a paradoxical suppressive effect of central GHRH action, and 3) peripheral SRIF withdrawal-induced rebound-like secretion of GH in the adult female rat (13,20,27,30,34,42).The present work formulates and implements an alternative model of GH autoregulation, which combines four distinct mechanisms: 1) long-loop, timedelayed stimulation of SRIF release by blood-borne GH (systemic-CNS control); 2) periventricular SRIF-dependent inhibition of pituitary GH release but not synthesis (CNS-pituitary regulation); 3) arcuate-nu- …”
mentioning
confidence: 99%
“…This two-oscillator formulation explicates (but does not prove) 1) the GHRH-sensitizing action of prior SRIF exposure; 2) a three-site (intrahypothalamic, hypothalamo-pituitary, and somatotrope GH store dependent) mechanism driving rebound-like GH secretion after SRIF withdrawal in the male; 3) an obligatory role for pituitary GH stores in representing rebound GH release in the female; 4) greater irregularity of SRIF than GH release profiles; and 5) a basis for the paradoxical GH-inhibiting action of centrally delivered GHRH. feedback; mathematical model; somatotropic axis; hormone pulsatility; somatostatin; growth hormone-releasing hormone; hypothalamus THE SECRETION OF GROWTH HORMONE (GH) is pulsatile in the human, monkey, sheep, swine, guinea pig, rat, and mouse (10,20,21,30,34,37,40,48,49). In the rodent, episodic GH release directs somatic growth, cellular gene expression, and autonegative feedback (3,20,31,34,37,42).…”
mentioning
confidence: 99%
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