Pituitary response to growth hormone-releasing factor in rats with functional or anatomical lesions of the central nervous system that inhibit endogenous growth hormone secretion

Wehrenberg, William B.; Bloch, Bertrand; Zhang, Chongli; Brazeau, Paul; Ling, Nicholas; Guillemin, Roger

doi:10.1016/0167-0115(84)90023-5

Cited by 14 publications

(5 citation statements)

References 32 publications

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“…A decrease in somatostatin activity may contribute to the effect of the steroid on GH responses to clonidine and GHRH (cf. Wehrenberg et al, 1984) and may also explain some of the apparently paradoxical results concerning the influence of estrogens on GH responsiveness to GHRH previously obtained using different experimental approaches (vide supra). However, testosterone did not increase base-line GH levels but was in males at least as effective as estradiol with respect to restoring the GH responsiveness to GHRH and clonidine.…”

Section: Discussionmentioning

confidence: 90%

“…The normal pulsatile secretion of GH in rat is totally suppressed after administration of reserpine in a dose causing depletion of brain monoamines (Eden et al, 1979); both a decrease in GHRH activity, caused by the absence of adrenergic alpha2-receptor activation (Eden et al, 1981), and an increase in the release of somatostatin (the hypothalamic GH inhibiting factor) (Eden et al, 1981;Wehrenberg et al, 1984) may contribute to this dramatic effect. In the present study all rats were pretreated with reserpine 5-6 h before the administration of clonidine or GHRH in order to eliminate presynaptic monoaminergic influence as well as to obtain a low, pulse-less base-line of serum GH from which a drug induced increase can be easily measured.…”

Section: Discussionmentioning

confidence: 96%

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Effects of sex steroids on growth hormone responses to clonidine and GHRH in reserpine pretreated rats

Eriksson

Modigh

Jansson

1988

J. Neural Transmission

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Administration of reserpine in a dose causing depletion of brain monoamines led to a complete suppression of the pulsatile secretory pattern of growth hormone (GH) in gonadectomized (GX) as well as in sham-operated male and female rats. In GX animals of both sexes treated with estradiol, but not in those treated with testosterone or dihydrotestosterone (DHT), the reserpine induced inhibition of GH release was partially antagonized. Administration of the alpha 2-adrenoceptor agonist clonidine caused secretion of GH in reserpine pretreated, sham-operated rats. In GX male rats GH responses to clonidine were blunted, while in GX males treated with testosterone or estradiol, but not in those treated with DHT, the responses were restored. In female rats gonadectomy did not significantly affect the GH releasing effect of clonidine. However, administration of estradiol to GX females led to enhanced responses to the alpha 2-agonist. Administration of the GH releasing hormone (GHRH) induced pronounced GH secretion in reserpine pretreated animals of both sexes; this effect was not significantly affected by gonadectomy. In GX males, however, GH responses to GHRH were enhanced by replacement with estradiol or testosterone, while in GX females, estradiol, but not testosterone, had the same effect.

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Section: Discussionmentioning

confidence: 90%

Section: Discussionmentioning

confidence: 96%

Effects of sex steroids on growth hormone responses to clonidine and GHRH in reserpine pretreated rats

Eriksson

Modigh

Jansson

1988

J. Neural Transmission

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“…A 5-HT influence on the alpha2-receptor / GHRF/ GH axis was proposed by Wehrenberg et al (1984) and a decreased 5-HT activity, such as shown in dementia disorders (Gottfries et al, 1970;Soininen et al, 1981;Parnetti et al, 1987), is reported to increase the release of the GHinhibiting factor (somatostatin), making the somatotrophs in the pituitary less responsive to GHRF but also to, for example, clonidine (Soderpalm et al, 1987). Yet the lack of significant correlations in this study between GH and the CSF levels of 5-HIAA as well as the fact that the 5-HT-stimulatory drug citalopram did not change the clonidine-GH responses does not support such an explanation in humans, at least in patients with dementia disorders.…”

Section: Discussionmentioning

confidence: 99%

The clonidine test in patients with dementia disorders: Relation to clinical status and cerebrospinal fluid metabolite levels

Balldin

Gottfries

Lindstedt

et al. 1988

Int J Geriat Psychiatry

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SUMMARYClonidine loading tests (100 pg i.v.) for growth hormone (GH) release were performed in eight patients with dementia of the Alzheimer type and four with multi-infarct dementia. Clonidine did not stimulate GH but depressed blood pressure levels. Basal GH levels correlated to clinical variables of affective symptomatology but not with monoamine levels in the cerebrospinal fluid. Treatment with a 5-HT uptake inhibitor (citalopram) did not affect the outcome of the loading tests.

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“…Der Vergleich zweier Variablen erfolgte mittels linearer Regressionsanalyse. (27). Die große Variabilität der WH-Antwort auf GHRH-Stimulation bei gesunden Probanden ist somit durch den unterschiedlichen SRIF-Tonus zum Zeitpunkt des exogen verabreichten GHRH erklärbar.…”

Section: Schlüsselwörter Wachstumshormonunclassified

Verhalten von Wachstumshormon nach Stimulation mit Wachstumshormon-Releasing-Hormon (GHRH) bei Kindern mit Störungen der Hypothalamus-Hypophysen-Achse und Mädchen mit Turner-Syndrom

Schimrigk¹,

Schober²,

Birnbacher³

et al. 1996

Klin Padiatr

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Pituitary GH secretion could be activated by repeated stimulation with GHRH (priming) in children with hypothalamic GH deficiency. Only in the patients with MPHD a correlation could be found between the result of the GHRH-stimulation and one pharmacological GH test. In children with OGHD the radiation dose was negatively correlated to the maximal GH concentrations after L-Dopa stimulation. Basal and GHRH stimulated GH levels in Turner syndrome were lower after estrogen administration.

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Pituitary response to growth hormone-releasing factor in rats with functional or anatomical lesions of the central nervous system that inhibit endogenous growth hormone secretion

Cited by 14 publications

References 32 publications

Effects of sex steroids on growth hormone responses to clonidine and GHRH in reserpine pretreated rats

Effects of sex steroids on growth hormone responses to clonidine and GHRH in reserpine pretreated rats

The clonidine test in patients with dementia disorders: Relation to clinical status and cerebrospinal fluid metabolite levels

Verhalten von Wachstumshormon nach Stimulation mit Wachstumshormon-Releasing-Hormon (GHRH) bei Kindern mit Störungen der Hypothalamus-Hypophysen-Achse und Mädchen mit Turner-Syndrom

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