Role of Nitric Oxide in Control of Growth Hormone Release in the Rat

Rettori, Valéria; Belova, N.; Yu, Wen H.; Gimeno, M.F.; McCann, Samuel M.

doi:10.1159/000097160

Cited by 43 publications

(23 citation statements)

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“…Our results are in agreement with theirs and indicate that NO has precious little effect on basal LH release from hemipituitaries; however, the paracrine actions of gonadotropes on prolactin secretion may be brought about by NO. From these studies, it is apparent that NO has important effects on the secretion of pituitary hormones not only by altering release of releasing hormones from the hypothamus but also by actions on the gland itself. In the case of prolactin, we have reported that injection of NMMA into the third brain ventricle had no effect on basal pulsatile prolactin release, but that it completely blocked the stimulation of prolactin release induced by injection into the third ventricle of interleukin-1 a subunit (IL-la) (9). We believe that this represents an action on the hypothalamus to suppress the secretion of prolactinreleasing factors induced IL-la.…”

Section: Discussionmentioning

confidence: 96%

Role of nitric oxide in control of prolactin release by the adenohypophysis.

Duvilanski

Zambruno

Seilicovich

et al. 1995

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

134

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Nitric oxide synthase-containing cells were visualized in the anterior pituitary gland by immunocytochemistry. Consequently, we began an evaluation of the possible role of NO in the control of anterior pituitary function.Prolactin is normally under inhibitory hypothalamic control, and in vitro the gland secretes large quantities of the hormone. When hemipituitaries were incubated for 30 min in the presence of sodium nitroprusside, a releaser of NO, prolactin release was inhibited. This suppression was completely blocked by the scavenger of NO, hemoglobin. Analogs of arginine, such as NG-monomethyl-L-arginine (NMMA, where NG is the terminal guanidino nitrogen) and nitroarginine methyl ester, inhibit NO synthase. Incubation of hemipituitaries with either of these compounds significantly increased prolactin release. Since in other tissues most of the actions of NO are mediated by activation of soluble guanylate cyclase with the formation of cyclic GMP, we evaluated the effects of cyclic GMP on prolactin release. Cyclic GMP (10 mM) produced an "40%o reduction in prolactin release. Prolactin release in vivo and in vitro can be stimulated by several peptides, which include vasoactive intestinal polypeptide and substance P. Consequently, we evaluated the possible role of NO in these stimulations by incubating the glands in the presence of either of these peptides alone or in combination with NMMA. In the case of vasoactive intestinal polypeptide, the significant stimulation of prolactin release was augmented by NMMA to give an additive effect. In the case of substance P, there was a smaller but significant release of prolactin that was not significantly augmented by NMMA. We conclude that NO has little effect on the stimulatory action of these two peptides on prolactin release. Dopamine (0.1 ,uM), an inhibitor of prolactin release, reduced prolactin release, and this inhibitory action was significantly blocked by either hemoglobin (20 jig/ml) or NMMA and was completely blocked by 1 mM nitroarginine methyl ester. Atrial natriuretic factor at 1 ,uM also reduced prolactin release, and its action was completely blocked by NMMA. In contrast to these results with prolactin, luteinizing hormone (LH) was measured in the same medium in which the effect of nitroprusside was tested on prolactin release, there was no effect of nitroprusside, hemoglobin, or the combination of nitroprusside and hemoglobin on luteinizing hormone release. Therefore, in contrast to its inhibitory action on prolactin release NO had no effect on luteinizing hormone release. Immunocytochemical studies by others have shown that NO synthase is present in the folliculostellate cells and also the gonadotrophs of the pituitary gland. We conclude that NO produced by either of these cell types may diffuse to the lactotropes, where it can inhibit prolactin release. NO appears to play little role in the The publication costs of this article were defrayed in part by page charge payment. This article must therefore be hereby marked "advertisement" in accorda...

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Section: Discussionmentioning

confidence: 96%

Role of nitric oxide in control of prolactin release by the adenohypophysis.

Duvilanski

Zambruno

Seilicovich

et al. 1995

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

134

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“…However, the mechanism by which NO influences GH secretion is still a matter of controversy. Pleiotropic effects on somatotropes increased GHRH secretion [14]and increased [15]or decreased [17]hypothalamic somatostatinergic tone has been postulated. Our data showing that L-NAME can block completely cGH secretion stimulated by GHRH are compatible with the hypothesis that NO acts by stimulating somatostatin release and/or by inhibiting cGH release at the pituitary level.…”

Section: Discussionmentioning

confidence: 99%

“…In this context, either facilitatory or inhibitory actions of NO on basal and/or stimulated GH release have been reported in vivo and in vitro [13, 14, 15]. Other data have indicated that appropriate NO supply is essential for full efficacy of different GH stimulators, such as GHRH, GHRP-6 or kainic acid [16, 17].…”

Section: Introductionmentioning

confidence: 99%

Involvement of Nitric Oxide in the Regulation of Growth Hormone Secretion in Dogs

et al. 2001

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Nitric oxide (NO) is a highly reactive gas that has been suggested to function as a neurotransmitter in the neuroendocrine system. In this work, we have evaluated the role of NO pathways in growth hormone (GH) secretion by assessing the effect of L-arginine infusion, a precursor of NO formation, and L-NAME, a nitric oxide synthase (NOS) inhibitor. The experiments were carried out on 7 adult beagle dogs. A saline infusion was carried out on all the dogs as a control test. L-arginine (infusion i.v. 10 g in 100 ml of saline, from t = 0 to 30 min) and L-nitro-arginine-methyl ester, L-NAME (infusion of 300 µg/kg in 120 ml of saline, from t = –30 to 45 min) were administered alone and together with growth hormone-releasing hormone (GHRH) (i.v. bolus at 0 min, at a dose of 100 µg), the synthetic GH secretagogue GHRP-6 (i.v. bolus at 0 min, at a dose of 90 µg), and the 5-HT1D serotonin receptor agonist sumatriptan, SUM (s.c. injection at the dose of 3 mg). Plasma cGH was determined by RIA. Results were evaluated by one-way analysis of variance, followed by the Newman-Keuls test for multiple comparisons. L-arginine administration resulted in a slight increase in plasma cGH in comparison with saline controls. Combined administration of L-arginine and GHRH enhanced cGH release in comparison with GHRH alone. L-NAME alone did not modify baseline cGH levels, but completely suppressed the GH release induced by GHRH or GHRP-6. It also strongly reduced, but did not abolish the effect of the two peptides (GHRH plus GHRP-6) administered together. Finally, administration of the 5-HT1D agonist SUM induced a significant cGH secretion in all dogs, a response which was not modified when L-NAME was administered in combination with SUM. In conclusion, our data show that inhibition of NO blunts both GHRH or GHRP-6-induced cGH release, and are compatible with the hypothesis that it acts by decreasing hypothalamic somatostatin release.

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“…NOergic neurons stimulate the release of a number of polypeptides from the hypothalamus including luteinizing hormone-releasing hormone (LHRH) (3), corticotropinreleasing hormone (4), somatostatin (5), growth hormonereleasing hormone (6), and prolactin-releasing factors (7).…”

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confidence: 99%

Nitric oxide inhibits hypothalamic luteinizing hormone-releasing hormone release by releasing gamma-aminobutyric acid.

Seilicovich

Duvilanski

Pisera

et al. 1995

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

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Nitric oxide synthase (NOS)-containing neurons, termed NOergic neurons, occur in various regions of the hypothalamus, including the median eminence-arcuate region, which plays an important role in controlling the release of luteinizing hormone-releasing hormone (LHRH). We examined the effect of NO on release of y-aminobutyric acid (GABA) from medial basal hypothalamic (MBH) explants incubated in vitro. Sodium nitroprusside (NP) (300 ,uM), a spontaneous releaser of NO, doubled the release of GABA. This release was significantly reduced by incubation of the tissue with hemoglobin, a scavenger of NO, whereas hemoglobin alone had no effect on the basal release of GABA. Elevation of the potassium concentration (40 mM) in the medium increased GABA release 15-fold; this release was further augmented by NP. Hemoglobin blocked the increase in GABA release induced by NP but had no effect on potassium-induced release, suggesting that the latter, is not related to NO. As in the case of hemoglobin, NG-monomethyl-L-arginine (NMMA), a competitive inhibitor of NOS, had no effect on basal release of GABA, which indicates again that NO is not significant to basal GABA release. However, NMMA markedly inhibited the release of GABA induced by high potassium, which indicates that NO plays a role in potassiuminduced release of GABA. In conditions in which the release of GABA was substantially augmented, there was a reduction in GABA tissue stores as well, suggesting that synthesis of GABA in these conditions did not keep up with release of the amine. Although NO released GABA, there was no effect of the released GABA on NO production, for incubation of MBH explants with GABA had no effect on NO release as measured by [14C]citrulline production. To determine whether GABA had any effect on the release of LHRH from these MBH explants, GABA was incubated with the tissue and the effect on LHRH release was determined. GABA (10-5 or 10-6 M) induced a 70%o decrease in the release of LHRH, indicating that in the male rat GABA inhibits the release of this hypothalamic peptide. This inhibition in LHRH release induced by GABA was blocked by NMMA (300 ,uM), which indicates that GABA converts the stimulatory effect of NO on LHRH release into an inhibitory one, presumably via GABA receptors, which activate chloride channels that hyperpolarize the cell. Previous results have indicated that norepinephrine stimulates release of NO from the NOergic neurons, which then stimulates the release of LHRH. The current results indicate that the NO released also induces release of GABA, which then inhibits further LHRH release. Thus, in vivo the norepinephrinergic-driven pulses of LHRH release may be terminated by GABA released from GABAergic neurons via NO.Constitutive nitric oxide synthase (NOS) occurs in hypothalamic neurons (1, 2). These neurons, which convert L-arginine to citrulline and NO, have been termed NOergic neurons (2,The publication costs of this article were defrayed in part by page charge payment. This article must therefore be hereby ma...

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Role of Nitric Oxide in Control of Growth Hormone Release in the Rat

Cited by 43 publications

References 0 publications

Role of nitric oxide in control of prolactin release by the adenohypophysis.

Role of nitric oxide in control of prolactin release by the adenohypophysis.

Involvement of Nitric Oxide in the Regulation of Growth Hormone Secretion in Dogs

Nitric oxide inhibits hypothalamic luteinizing hormone-releasing hormone release by releasing gamma-aminobutyric acid.

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