GH release

B16. van den Berghe, G., de Zegher, F Veldhuis, J. D., Wouters, P Awouters, M Verbruggen, W., Schetz, M Verwaest, C Lauwers, R, Bouillon, R and Bowers, C. Y., The somatotropic axis in critical illness Effect of continous growth hormone (GH)-releasing hormone and GH-re-leasing peptide-2 infusion. J. Clin. Endocrinol. Metab. 82,590-599 (1997). 

Table 8.5. Some factors known to affect the rate of secretion of GH. Most of these factors influence GH release indirectly by affecting the rate and level of secretion of GHRH and/or GHRIH...

Dopamine agonists suppress prolactin release very effectively in patients with hyperprolactinemia. GH release is reduced in patients with acromegaly, although not as effectively. Cabergoline and bromocriptine are also used in Parkinson s disease to improve motor function and reduce levodopa requirements (see Chapter 28). Newer, nonergot D2 agonists... 

Few studies have evaluated the effect of HA on GH secretion. Central administration of HA inhibits basal and stimulated GH release predominantly via activation of HI receptors [58,60-61], whereas systemic injection of HA seem to stimulate GH secretion either via HI or H2 receptors [62-63], Following both administration routes, the effect of HA is indirect presumably mediated by activation of GHRH or other GH releasing factors but presumably not via somatostatin [63-64],... 

Effects of recombinant human growth hormone (GH) on bone and intermediary metabolism in patients receiving chronic glucocorticoid treatment with suppressed endogenous GH response to GH-releasing hormone. J Clin Endocrinol Metab 1995 80(l) 122-9. 

When GH was utilized with an insulin protocol, it was considered important to space injection periods between GH and insulin about an hour. Also if GH was utilized only twice daily, it was reported best to avoid natural high points of GH release such as first thing in the a.m., post-work out, and right before bed. This was if GH was utilized without insulin. 

Growth hormone-releasing hormone (GHRH] T GH release... 

Growth hormone-inhibitory hormone (GHIH] 4- GH release... 

GH release [52], that dexamethasone, which increases the GH response to GRF, also increases the stimulation of cAMP accumulation by GRF but not basal levels [54] and that the ED,() of increasing GH (1.6 x 10 12 M) closely matches the ED5() of increasing cAMP levels (6 x 10 12 M). The increase of cAMP levels is caused by a stimulation of the adenylate cyclase in a GTP-dependent manner [55]. 

The GH release inhibitory action of SRIF at least in part involves inhibition of adenylate cyclase [55,56]. Most likely this occurs through coupling with the inhibitory regulatory G protein of the enzyme, since the effect is GTP-dependent and is blocked by pertussis toxin. However, in sheep cells SRIF inhibits GRF-stimulated GH release without any effect on cAMP levels whereas in rats GRF stimulation of GH is completely inhibited by SRIF but cAMP accumulation only in part [57], An additional site of action of SRIF appears to be at the level of GRF-stimulated Ca2+ mobilization (see below). 

GRF-stimulated GH release is also inhibited by lipoxygenase inhibitors, suggesting participation of some lipoxygenase product(s). However, in this area of research more work is also required to attribute a specific messenger role to these arachidonic acid metabolites. 

Dose-response curves are established for standard and test compounds measuring GH release into the medium and GH depletion from the pituitaries. Potencies ratios with confidence limits are calculated from dose-concentration curves. 

GH release was determined using cultured rat pituitary cells (Brazeau et al. 1982 Perkins et al. 1983 Scheikl-Lenz et al. 1985). Pituitary cells were prepared by enzyme dispersion with collagenase, DNAase and pancreatin. The cells were cultured for 3 days in microbiological Petri dishes in Dulbecco s modified essential medium with 20 mM HEPES, 15 % fetal calf serum, 100 mU/ml penicillin-G and 100 (ig/ml streptomycin at 37 °C and 10 % C02. 

Regulation of growth harmone (GH) secretion in mammals involves a complex interaction between inhibitory (somatostatin) and stimulatory (GH releasing hormone GHRH) neuropeptides synthesized and released by neurosecretory neurons terminating in the median eminence (Tuomisto and Mannisto, 1985 McMahon et al., 2001). Somatostatin and GHRH are transported in the hypophysial portal blood to the anterior pituitary... 

Kakucska I, Makara GB (1983) Various putative neurotransmittere affect growth hormone (GH) release in rats with anterolateral hypothalamic deafferentation of the medial basal hypothalamus evidence for mediation by a GH-releasing factor. Endocrinology 775 318-323. 

Lindstrom P, Ohlsson L (1987) Effects of 5-hydroxytryptamine, dopamine, and aromatic L-amino acids on growth hormone (GH)-releasing factor-stimulated GH release in rat anterior pituitaries. Endocrinology 720 780-784. 

Tannenbaum GS, Ling N (1984) The interrelationship of growth hormone (GH)-releasing factor and somatostatin in generation of the ultradian rhythm of GH secretion. Endocrinology 775 1952-1957. 

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