Luteinizing hormone response to an intravenous infusion of substance P in normal men

Coiro, V.; Volpi, R.; Caiazza, A.; Marcato, A.; Bocchi, R.; Colla, Rossana; Rossi, G.; Chiodera, P.

doi:10.1016/0026-0495(92)90305-t

Cited by 28 publications

(26 citation statements)

References 23 publications

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“…Furthermore, KNDy cells are interconnected with NKB fibers within the ARC forming a tightly regulated network (Rance & Bruce 1994, Krajewski et al 2010. Indeed, a growing number of studies in multiple species from our lab and others support the ability of NKB, or the NKB receptor (NK3R) agonist senktide, to increase LH pulses (Grachev et al 2012, Navarro 2013, Goodman et al 2014 (Arisawa et al 1990, Kalra et al 1992, Sahu & Kalra 1992, Noritake et al 2011, de Croft et al 2013 including men (Coiro et al 1992). It is therefore plausible to speculate that these tachykinins are involved in the central regulation of GnRH release and may be additional elements to the GnRH pulse generator.…”

Section: The Current Model For the Gnrh Pulse Generatormentioning

confidence: 99%

“…These include peripheral (i.v.) administration of SP for 1 hour in normal men, which induced a robust discharge of LH (Coiro et al 1992), and in OVX rats, i.c.v.-specific antiserum against SP (anti-SP) decreased plasma LH, whereas synthetic SP injected i.c.v. or i.v.…”

Section: Substance Pmentioning

confidence: 99%

“…Early studies documented a robust stimulatory action of LH release by SP in rats, rabbits and humans (Arisawa et al 1990, Coiro et al 1992, Kalra et al 1992, Sahu & Kalra 1992, Traczyk et al 1992, and recent electrophysiological studies have described potent depolarizing effects of SP and NKA on ARC Kiss1 neurons in the mouse (de Croft et al 2013) indicating that LH stimulation by these tachykinins involves, at least in part, a kisspeptin-dependent mechanism. Of note, this study showed that, in vitro, the activation of kisspeptin neurons by NKB was completely diminished only when all three neurokinin receptor (NKR) subtypeselective antagonists were concomitantly applied in the in vitro bath (de Croft et al 2013).…”

Section: Introductionmentioning

confidence: 99%

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Expanding the role of tachykinins in the neuroendocrine control of reproduction

Fergani

Navarro

2017

Reproduction

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Reproductive function is driven by the hormonal interplay between the gonads and brain-pituitary axis. Gonadotropin-releasing hormone (GnRH) is released in a pulsatile manner, which is critical for the attainment and maintenance of fertility; however, GnRH neurons lack the ability to directly respond to most regulatory factors, and a hierarchical upstream neuronal network governs its secretion. We and others proposed a model in which Kiss1 neurons in the arcuate nucleus (ARC), called as KNDy neurons, release kisspeptin (a potent GnRH secretagogue) in a pulsatile manner to drive GnRH pulses under the coordinated autosynaptic action of its cotransmitters, the tachykinin neurokinin B (NKB, stimulatory) and dynorphin (inhibitory). Numerous genetic and pharmacological studies support this model; however, additional regulatory mechanisms (upstream of KNDy neurons) and alternative pathways of GnRH secretion (kisspeptin independent) exist, but remain ill defined. In this aspect, attention to other members of the tachykinin family, namely substance P (SP) and neurokinin A (NKA), has recently been rekindled. Even though there are still major gaps in our knowledge about the functional significance of these systems, substantial evidence, as discussed below, is placing tachykinin signaling as an important pathway for the awakening of the reproductive axis and the onset of puberty to physiological GnRH secretion and maintenance of fertility in adulthood.Reproduction (2017) 153 R1-R14

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Section: The Current Model For the Gnrh Pulse Generatormentioning

confidence: 99%

Section: Substance Pmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Expanding the role of tachykinins in the neuroendocrine control of reproduction

Fergani

Navarro

2017

Reproduction

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“…Intravenous administration of substance P at 1.5 pmol/kg/min for 60 min (approximately a total infusion of 7 nmol of substance P) resulted in an approximate doubling of plasma LH levels during the infusion in healthy men [31]. Twenty minutes after the end of the infusion of substance P, plasma LH levels had returned to baseline values.…”

Section: Administration Of Kisspeptin-54 To Humansmentioning

confidence: 96%

The neuroendocrine physiology of kisspeptin in the human

Dhillo

Murphy

Bloom

2007

Rev Endocr Metab Disord

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Kisspeptin is a 54-amino acid peptide, encoded by the KiSS-1 gene, which activates the G protein-coupled receptor GPR54. Recent evidence suggests the kisspeptin/GPR54 system is a key regulator of reproduction. GPR54-deficient mice have abnormal sexual development. Central or peripheral administration of kisspeptin stimulates the hypothalamic-pituitary-gonadal (HPG) axis in animal models. This review discusses the evidence that kisspeptin also plays a key role in human reproduction. Inactivating GPR54 mutations cause normosmic hypogonadotrophic hypogonadism in humans. Mutations which increase GPR54 signaling are associated with gonadotrophin-dependent premature puberty. Acute intravenous administration of kisspeptin to healthy human male volunteers potently increased plasma LH levels and significantly increased plasma FSH and testosterone without side effects. Plasma kisspeptin is found at low concentrations in the circulation of men and non-pregnant women, but is markedly increased in pregnancy. The placenta is believed to be the source of these high levels of circulating kisspeptin. The kisspeptin-GPR54 system is also implicated in tumour biology. Consistent with this role, plasma kisspeptin concentrations are elevated in patients with abnormal proliferation of placental tissue (gestational trophoblastic neoplasia or GTN) at presentation and fall after treatment with chemotherapy. The kisspeptin/GPR54 system therefore appears to play an important role in the regulation of reproduction in humans. Kisspeptin represents a novel tool for the manipulation of the HPG axis in humans and plasma kisspeptin may be a novel tumour marker in patients with GTN.

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“…SP was given in a range of doses (0.5-1.5 pmol/kg-'/min-1) that did not produce stressful side effects and/or variations in blood pressure [1], In these experimental conditions, SP stimulated arginine vasopressin but not oxytocin secretion from the posterior pituitary [2], and G H [3]. A CT H [4] and LH [5] secretion from the anterior pituitary. In addition.…”

Section: Introductionmentioning

confidence: 99%

Intravenously Infused Substance P Is Unable to Change Basal and TRH-Stimulated PRL Secretion in Normal Men

Coiro

Volpi²,

Capretti³

et al. 1993

Horm Res

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In order to test the possible effects of an intravenous administration of substance P (SP) on basal and TRH-stimulated PRL release, SP was infused alone (0.5 or 1.5 pmol/kg^-1/min^-1 for 60 min) or after TRH (20 or 400 µg in an i.v. bolus) in 21 normal male subjects. In addition, plasma cortisol levels during SP infusion were measured. In agreement with previous findings, a significant increase in plasma cortisol levels was observed when the higher (1.5pmol/ kg^-1/min^-1) but not the lower (0.5 pmol/kg^-1/min^-1) amount of SP was given. In contrast, basal and TRH (20 or 400 µg)-induced PRL release were not modified by SP at any tested amount. These data suggest that, in normal men, plasma SP is not involved in the control of PRL release at the anterior pituitary level.

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Luteinizing hormone response to an intravenous infusion of substance P in normal men

Cited by 28 publications

References 23 publications

Expanding the role of tachykinins in the neuroendocrine control of reproduction

Expanding the role of tachykinins in the neuroendocrine control of reproduction

The neuroendocrine physiology of kisspeptin in the human

Intravenously Infused Substance P Is Unable to Change Basal and TRH-Stimulated PRL Secretion in Normal Men

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