Role of substance P in suppressing growth hormone release in the rat.

Arisawa, Masayoshi; Snyder, Gary D.; Palatis, L. De; Ho, Raymond H.; Xu, Ruiyi; Pan, George; McCann, Samuel M.

doi:10.1073/pnas.86.18.7290

Cited by 10 publications

(6 citation statements)

References 22 publications

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“…Second, a number of investigators have demonstrated the presence of nerve fibers within the anterior pituitary gland of the rat. These nerve fibers are immunoreactive for factors involved in pituitary regulation, such as substance P (1,23,30), calcitonin gene-related peptide (12,22,23), somatostatin (23,35), and serotonin (26). Furthermore, these nerve fibers lie in contact with, or in close apposition to, somatotrophs (27,35), thyrotrophs (35), and corticotrophs (22,24,27), and some respond to changes in the overall hormonal state of the animal (e.g., increasing density of varicosities near corticotrophs after adrenalectomy) (22,24,27).…”

Section: Discussionmentioning

confidence: 99%

Afferent input from rat slow skeletal muscle inhibits bioassayable growth hormone release

Gosselink

Grindeland

Roy

et al. 2000

Journal of Applied Physiology

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The release of a bioassayable form of growth hormone (BGH), distinct from growth hormone as measured by immunoassay (IGH), from the rat pituitary into the blood is differentially regulated by afferent input from fast and slow skeletal muscles. Specifically, activation of low-threshold fast muscle afferents for 15 min increased plasma BGH by 217 and 295% and decreased pituitary BGH by 68 and 45% in male and female rats, respectively. In contrast, activation of slow muscle afferents inhibited BGH release, decreasing plasma BGH by approximately 60% and increasing pituitary BGH by 30-50% in male rats. Female rats from which food had been withheld for approximately 12 h had elevated basal plasma BGH levels, which then were decreased by 81% after slow muscle nerve stimulation. Plasma IGH concentrations were unchanged after any nerve stimulation condition. These results demonstrate that regulation of BGH release can be differentially mediated through low-threshold afferent inputs from fast or slow skeletal muscle. Furthermore, the results indicate that BGH responses are independent of gender or feeding status.

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Section: Discussionmentioning

confidence: 99%

Afferent input from rat slow skeletal muscle inhibits bioassayable growth hormone release

Gosselink

Grindeland

Roy

et al. 2000

Journal of Applied Physiology

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“…GHRH is known to increase Substance P in the pituitary ( 460 ). The significance of these findings is unknown but is intriguing considering that Substance P was found to be ineffective with respect to in vitro GH secretion ( 457 , 461 ).…”

Section: Autocrine Regulation Of Somatotrophsmentioning

confidence: 99%

Paracrinicity: The Story of 30 Years of Cellular Pituitary Crosstalk

Denef

2007

J Neuroendocrinology

213

238

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Living organisms represent, in essence, dynamic interactions of high complexity between membrane‐separated compartments that cannot exist on their own, but reach behaviour in co‐ordination. In multicellular organisms, there must be communication and co‐ordination between individual cells and cell groups to achieve appropriate behaviour of the system. Depending on the mode of signal transportation and the target, intercellular communication is neuronal, hormonal, paracrine or juxtacrine. Cell signalling can also be self‐targeting or autocrine. Although the notion of paracrine and autocrine signalling was already suggested more than 100 years ago, it is only during the last 30 years that these mechanisms have been characterised. In the anterior pituitary, paracrine communication and autocrine loops that operate during fetal and postnatal development in mammals and lower vertebrates have been shown in all hormonal cell types and in folliculo‐stellate cells. More than 100 compounds have been identified that have, or may have, paracrine or autocrine actions. They include the neurotransmitters acetylcholine and γ‐aminobutyric acid, peptides such as vasoactive intestinal peptide, galanin, endothelins, calcitonin, neuromedin B and melanocortins, growth factors of the epidermal growth factor, fibroblast growth factor, nerve growth factor and transforming growth factor‐β families, cytokines, tissue factors such as annexin‐1 and follistatin, hormones, nitric oxide, purines, retinoids and fatty acid derivatives. In addition, connective tissue cells, endothelial cells and vascular pericytes may influence paracrinicity by delivering growth factors, cytokines, heparan sulphate proteoglycans and proteases. Basement membranes may influence paracrine signalling through the binding of signalling molecules to heparan sulphate proteoglycans. Paracrine/autocrine actions are highly context‐dependent. They are turned on/off when hormonal outputs need to be adapted to changing demands of the organism, such as during reproduction, stress, inflammation, starvation and circadian rhythms. Specificity and selectivity in autocrine/paracrine interactions may rely on microanatomical specialisations, functional compartmentalisation in receptor–ligand distribution and the non‐equilibrium dynamics of the receptor–ligand interactions in the loops.

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“…Central administration of SP rapidly raised plasma GH in ovariectomized rats (Vijayan & McCann, 19796), and Kakucska & Makara (1983) also reported a stimulatory effect but only after deafferentation of the somatostatinergic input to the hypothalamus. However, more recent evidence suggests that centrally administered SP can also inhibit the release of GH in conscious rats (Arisawa, Snyder, De Palatis et al 1989), and a decrease (unconvincing) has been observed in primates (Eckstein et al 1980). These apparently contradictory results may be reconciled by the doses used and the influence of anaesthesia.…”

Section: Introductionmentioning

confidence: 97%