Growth Hormone (Gh) Responses to Arginine and L‐dopa Alone and After GHRH Pretreatment

Page, M. D.; Diéguez, Carlos; Valcavi, Roberto; Edwards, C.; Hall, R.; Scanlon, M. F.

doi:10.1111/j.1365-2265.1988.tb03690.x

Cited by 60 publications

(34 citation statements)

References 21 publications

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“…The present study demonstrates that GHRH potentiate Arg-induced GH secretion, while Arg-priming markedly suppresses GHRH-induced GH release. A similar enhancing effect of GHRH pretreatment on Arg-induced GH secretion was reported by Page et al (1988). Since these effects were repeatedly observed in the same subjects on different days, it is unlikely that the mutual potentiating or suppressing effect is due to occasional coincidence with endogenous GHRH-SRIH release.…”

Section: Discussionsupporting

confidence: 77%

Mutual Priming Effects of GHRH and Arginine on GH Secretion: Informative Procedure for Evaluating GH Secretory Dynamics.

et al. 1990

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Section: Discussionsupporting

confidence: 77%

Mutual Priming Effects of GHRH and Arginine on GH Secretion: Informative Procedure for Evaluating GH Secretory Dynamics.

et al. 1990

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“…The second postulate conforms with the fact that the FUL effect was exerted on GH secretion stimulated by GHRH/ GHRP-2, but not L-arginine/GHRH or L-arginine/GHRP-2. The reason is that L-arginine inhibits GH-induced SS outflow (1,36), which would inferentially mask any upregulation of SSTR-2.…”

Section: Discussionmentioning

confidence: 99%

“…A consideration is that L-arginine, by repressing GH feedback-induced SS outflow to the pituitary gland (1,36), limits detection of any effects of E 2 and/or FUL on pituitary SS receptors. However, E 2 abbreviated GH secretory bursts induced by L-arginine/ GHRP-2.…”

Section: Discussionmentioning

confidence: 99%

Peripheral estrogen receptor-α selectively modulates the waveform of GH secretory bursts in healthy women

Veldhuis¹,

Keenan²,

Bowers³

2007

American Journal of Physiology-Regulatory, Integrative and Comp

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Veldhuis JD, Keenan DM, Bowers CY. Peripheral estrogen receptor-␣ selectively modulates the waveform of GH secretory bursts in healthy women. Am J Physiol Regul Integr Comp Physiol 293: R1514-R1521, 2007. First published August 8, 2007; doi:10.1152 doi:10. /ajpregu.00438.2007 drives growth hormone (GH) secretion via estrogen receptors (ER) located in the hypothalamus and pituitary gland. ER␣ is expressed in GH releasing hormone (GHRH) neurons and GH-secreting cells (somatotropes). Moreover, estrogen regulates receptors for somatostatin, GHR peptide (GHRP, ghrelin), and GH itself, while potentiating signaling by IGF-I. Given this complex network, one cannot a priori predict the selective roles of hypothalamic compared with pituitary ER pathways. To make such a distinction, we introduce an investigative model comprising 1) specific ER␣ blockade with a pure antiestrogen, fulvestrant, that does not penetrate the blood-brain barrier; 2) graded transdermal E 2 administration, which doubles GH concentrations in postmenopausal women; 3) stimulation of fasting GH secretion by pairs of GHRH, GHRP-2 (a ghrelin analog), and L-arginine (to putatively limit somatostatin outflow); and 4) implementation of a flexible waveform deconvolution model to estimate the shape of secretory bursts independently of their size. The combined strategy unveiled that 1) E 2 prolongs GH secretory bursts via fulvestrant-antagonizable mechanisms; 2) fulvestrant extends GHRH/GHRP-2-stimulated secretory bursts; 3) L-arginine/GHRP-2 stimulation lengthens GH secretory bursts whether or not E 2 is present; 4) E2 limits the capability of L-arginine/GHRP-2 to expand GH secretory bursts, and fulvestrant does not inhibit this effect; and 5) E 2 and/or fulvestrant do not alter the time evolution of L-arginine/GHRH-induced GH secretory bursts. The collective data indicate that peripheral ER␣-dependent mechanisms determine the shape (waveform) of in vivo GH secretory bursts and that such mechanisms operate with secretagogue selectivity. somatotropin; ghrelin; growth hormone releasing hormone; somatostatin; secretagogues; female; human GROWTH HORMONE (GH) secretion is at least 90% pulsatile in the healthy human and strongly controlled by sex steroid hormones (17,19). Individual GH secretory bursts are believed to reflect the concerted effects of somatotrope stimulation by GH-releasing hormone (GHRH), inhibition by somatostatin (SS), and amplification by the potent GHR peptide (GHRP) ghrelin (14,45). Estrogen supplementation stimulates pulsatile GH secretion in postmenopausal women and girls with ovarian dysgenesis (32, 38). Putative mechanisms include the capability of estradiol (E 2 ) to potentiate GHRH drive (reduce the halfmaximally stimulatory dose), augment GHRP stimulation (increase apparent efficacy), and antagonize SS inhibition (increase the half-maximally inhibitory dose) (2, 5, 41, 43). The topographic sites at which estrogen exerts such effects are not known (45). However, E 2 can upregulate pituitary SS-type 2 and hypothalamic GHRP receptors and...

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“…A potentiating effect between ARG and GHRH on GH release has been described in human (Alba-Roth et al, 1988;Page et al, 1988;Ghigo et al, 1990bGhigo et al, , 1991Ghigo et al, , 1992Ghigo et al, , 1994) except with children of short stature (Ghigo et al, 1990a …”

mentioning

confidence: 99%

“…ARG probably acting by inhibiting somatostatin release from the hypothalamus is able to enhance GH response to GHRH in human (Alba-Roth et al, 1988;Page et al, 1988;Ghigo et al, 1990aGhigo et al, , b, 1991Ghigo et al, , 1992Ghigo et al, , 1994 (Louveau et al, 1991) using a specific antibody raised in rabbit (UCB Bioproducts, Brussels, Belgium).…”

mentioning

confidence: 99%

Effects of arginine, growth hormone-releasing hormone (GHRH) and neostigmine administered singly or in paired combinations on growth hormone (GH) release in pigs

Cochard¹,

Guilhermet²,

Bonneau³

1997

Reprod. Nutr. Dev.

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Summary -In human, arginine (ARG) induces growth hormone (GH) release, probably via a decrease in somatostatinergic tone. To assess the mechanism by which ARG mediates GH release in pigs, the effects on plasma GH release of ARG ( 1 g/kg body weight, infused between times -15 and -5 min), growth hormone-releasing hormone (GHRH, 2 pg/kg, at time 0 min) and neostigmine, a cholinesterase inhibitor (NEO, 50 arginine / growth hormone-releasing hormone / néostigmine / hormone de croissance / porc

show abstract

Growth Hormone (Gh) Responses to Arginine and L‐dopa Alone and After GHRH Pretreatment

Cited by 60 publications

References 21 publications

Mutual Priming Effects of GHRH and Arginine on GH Secretion: Informative Procedure for Evaluating GH Secretory Dynamics.

Mutual Priming Effects of GHRH and Arginine on GH Secretion: Informative Procedure for Evaluating GH Secretory Dynamics.

Peripheral estrogen receptor-α selectively modulates the waveform of GH secretory bursts in healthy women

Effects of arginine, growth hormone-releasing hormone (GHRH) and neostigmine administered singly or in paired combinations on growth hormone (GH) release in pigs

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