Inhibition of adenosine 3′,5′-monophosphate accumulation in anterior pituitary gland in vitro by growth hormone-release inhibiting hormone

Borgeat, Pierre; Labrie, Fernand; Drouin, Jacques; Bélanger, Alain; Immer, H.; Sestanj, K.; Nelson, V.; Götz, Manfred; Schally, Andrew V.; Coy, David H.; Coy, Esther J.

doi:10.1016/s0006-291x(74)80295-0

Cited by 157 publications

(24 citation statements)

References 9 publications

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“…Available data indicate that at least two effects may be involved: one would be the level of cyclic AMP in the target cells, the other calcium uptake by these cells. Somatostatin suppressed basal as well as (prostaglandin, theophylline, TRH) stimulated levels of cyclic AMP in the pituitary gland and its cells [52, 9,10]. Our studies on isolated pancreatic islets from the rat also demonstrated a decrease in the level of ; o.,.. O0 MIN From Uvn~is-Wallensten et al [104] cyclic AMP [30,19].…”

Section: Mode Of Action Of Somatostatinmentioning

confidence: 78%

Somatostatin — both hormone and neurotransmitter?

1978

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Section: Mode Of Action Of Somatostatinmentioning

confidence: 78%

Somatostatin — both hormone and neurotransmitter?

1978

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“…Somatostatin has been shown to be effective in inhibiting the hormone stimulation in many [3,19,20] but not all tissues [21]. To our knowledge, this is the first demonstration of an inhibitory effect of somatostatin on the anti~uretic hormone-stimulated adenlyate cyclase.…”

Section: Discussionmentioning

confidence: 86%

“…Incubation time was 20min at 30°C. The reaction was stopped as in [19] and cyclic [32P]AMP searated according to [14]. Sources of all materials were as in 1151.…”

Section: Adeny~ate Cycfuse Assaymentioning

confidence: 99%

Inhibition by somatostatin of the vasopressin‐stimulated adenylate cyclase in a kidney‐derived line of cells grown in defined medium

Roy

1984

FEBS Letters

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LLC-PI& celIs, a kidney-derived cell line grown in defined medium, possess a vasopressin-sensitive adenylate cyclase. Somatostatin was able to inhibit the vasopressin-induced increase in adenylate cyclase activity, without affecting the basal enzyme activity. This inhibition was competitive. No effect of somatostatin could be detected on [3H]vasopressin binding suggesting an interaction of somatostatin with the vasopressin-sensitive system distal to the hormone-receptor interaction. At variance with N6-L-2-phenylisopropyladenosine (PIA), CTP did not potentiate the inhibition by somatostatin. The inhibition of the vasopressin stimulation by somatostatin and that by PIA were additive. Changing the composition of the cell growth medium increased the number of vasopressin receptors per cell. Cells with a high number of vasopressin receptors were less sensitive to inhibition by somatostatin. Such results suggested that somatostatin and vasopressin receptors and/or the inhibitory (Ni) and stimulatory (Ns) regulatory transducing components are regulated by different mechanisms. Somatostaiin VasopressinCell culture

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“…Intracellular cAMP levels are elevated within 1-5 min of the addition of GHRH to cultured pituitary cells (4,5,11), and extracellular cAMP accumulation is also enhanced. In previous studies, cAMP production and adenylate cyclase activity were reported to be attenuated by SS-14 (3)(4)(5)(12)(13)(14). It was also stated that the presence of extracellular Ca2+ is necessary for the mechanism of action of GHRH and that GHRH elicits a rapid increase in the intracellular Ca21 concentration, with peak levels occurring within 30 sec (9,(15)(16)(17).…”

Section: Discussionmentioning

confidence: 96%

Growth hormone-releasing hormone stimulates cAMP release in superfused rat pituitary cells.

Horváth¹,

Groot²,

Schally³

1995

Proc. Natl. Acad. Sci. U.S.A.

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The release of growth hormone (GH) and cAMP was studied in superfused rat pituitary cells by infusing growth hormone-releasing hormone (GHRH) at different doses or a combination of GHRH and somatostatin 14 . Threeminute pulses ofGHRH caused a dose-dependent GH and cAMP release (effective concentration of 50% of the maximal biological effect is 0.21 nM and 52.5 nM, respectively). The lowest effective doses of GHRH in the superfusion system were 0.03 nM for GH release and 0.3 nM for cAMP discharge when 3-min pulses were applied. The secretion of growth hormone (GH) from the somatotrophs of the pituitary gland is controlled primarily by two hypothalamic peptide hormones, growth hormone-releasing hormone (GHRH) and somatostatin 14 (SS-14). GHRH not only stimulates the secretion of GH from the anterior pituitary, but it also stimulates adenylate cyclase activity and cAMP production. Numerous studies support the hypothesis that the effect of GHRH is mediated by cAMP (1-4). Previous investigations on the role of cAMP in the GHRH-induced GH release were carried out in static incubation systems by using freshly dispersed or cultured pituitary cells. In most cases only the intracellular changes in cAMP were detected at different intervals after stimulation. Extracellular discharge of cAMP was determined in a few cases (4-6); however, the release of cAMP in a dynamic system has not been previously examined in parallel with GH release. The aim of our study was to investigate the time course of both GH and cAMP secretion in a superfusion system after infusing GHRH or a combination of GHRH and SS-14 at different doses. MATERIALS AND METHODSPeptides. Human GHRH-(1-29)NH2 (DBO-2-048-1) was synthesized and purified in our laboratory. SS-14 was obtained from Wyeth.Superfusion. The preparation of the cells and the superfusion system have been described (7,8). Two or three columns, each containing pituitary cells from three male SpragueDawley rats (180-220 g) were perfused simultaneously. Sample collection was started immediately with 9-min samples in the first 90 min of the experiments and 3-min samples, thereafter. The flow rate was 20 ml/h. The test samples were prepared from the stock solutions immediately before use. The void volume of the system was calibrated to 1 ml. The cells were stimulated with 3-min pulses of GHRH (from 0.01 nM to 10 ,M). The desensitizing effect of GHRH was examined during 2-h infusions of 0.1 nM or 1 nM GHRH. To avoid the oxidation of GHRH in the tissue culture medium, test samples were freshly diluted every 15 min during the 2-h period. The results are based on 10 independent experiments, and similar experimental designs were repeated 2-5 times.RIAs. GH was determined by RIA with materials provided by the National Hormone and Pituitary Program (NHPP, Rockville, MD) (ratGH-RP-2/AFP-3910B/, ratGH-I-6/AFP-5676B/, and anti-ratGH-RIA-5/AFP-411S/). For cAMP determination, the samples were acetylated with triethylamine/acetic anhydride (2:1; 25 ,ul per 500 ,ul of sample), and 2'-O-monosuccinyl-cAMP ...

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Inhibition of adenosine 3′,5′-monophosphate accumulation in anterior pituitary gland in vitro by growth hormone-release inhibiting hormone

Cited by 157 publications

References 9 publications

Somatostatin — both hormone and neurotransmitter?

Somatostatin — both hormone and neurotransmitter?

Inhibition by somatostatin of the vasopressin‐stimulated adenylate cyclase in a kidney‐derived line of cells grown in defined medium

Growth hormone-releasing hormone stimulates cAMP release in superfused rat pituitary cells.

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