Release of vasopressin and oxytocin by excitatory amino acid agonists and the effect of antagonists on release by muscarine and hypertonic saline, in the rat <i>in vivo</i>

Bisset, G. W.; Fairhall, K. M.

doi:10.1111/j.1476-5381.1996.tb15192.x

Cited by 13 publications

(11 citation statements)

References 30 publications

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“…High sodium excretion is in part a consequence of the natriuretic effect of plasma oxytocin, which was also found to be elevated. These data confirm previous studies which showed that OT is released after hyperosmotic stimulus [41]–[43].…”

Section: Discussionsupporting

confidence: 93%

Body Sodium Overload Modulates the Firing Rate and Fos Immunoreactivity of Serotonergic Cells of Dorsal Raphe Nucleus

et al. 2013

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In order to determine whether serotonergic (5HT) dorsal raphe nucleus (DRN) cells are involved in body sodium status regulation, the effect of a s.c. infusion of either 2 M or 0.15 M NaCl on 5HT DRN neuron firing was studied using single unit extracellular recordings. In separate groups of 2 M and 0.15 M NaCl-infused rats, water intake, oxytocin (OT) plasma concentration, urine and plasma sodium and protein concentrations were also measured. Also, to determine the involvement of particular brain nuclei and neurochemical systems in body sodium overload (SO), animals from both groups were perfused for brain immunohistochemical detection of Fos, Fos-OT and Fos-5HT expression. SO produced a significant increase in serotonergic DRN neuron firing rate compared to baseline and 0.15 M NaCl-infused rats. As expected, 2 M NaCl s.c. infusion also induced a significant increase of water intake, diuresis and natriuresis, plasma sodium concentration and osmolality, even though plasma volume did not increase as indicated by changes in plasma protein concentration. The distribution of neurons along the forebrain and brainstem expressing Fos after SO showed the participation of the lamina terminalis, extended amygdala, supraoptic and paraventricular hypothalamic nuclei in the neural network that controls osmoregulatory responses. Both Fos-OT immunoreactive and plasma OT concentration increased after s.c. hypertonic sodium infusion. Finally, matching the “in vivo” electrophysiological study, SO doubled the number of Fos-5HT immunolabeled cells within the DRN. In summary, the results characterize the behavioral, renal and endocrine responses after body sodium overload without volume expansion and specify the cerebral nuclei that participate at different CNS levels in the control of these responses. The electrophysiological approach also allows us to determine in an “in vivo" model that DRN 5HT neurons increase their firing frequency during an increase in systemic sodium concentration and osmolality, possibly to modulate sodium and water intake/excretion and avoid extracellular volume expansion.

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Section: Discussionsupporting

confidence: 93%

Body Sodium Overload Modulates the Firing Rate and Fos Immunoreactivity of Serotonergic Cells of Dorsal Raphe Nucleus

et al. 2013

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“…This phenomenon was partially reversed after retrodialysis of V 1 receptor antagonists ( 37). The opposite action of excitatory amino acids agonists, both under basal conditions or after osmotic stimulation, on hypothalamic release (our findings) and pituitary vasopressin release ( 5, 6, 9, 10) is consistent with these observations. A comparable phenomenon may be involved in the regulation of ACTH secretion.…”

Section: Discussionsupporting

confidence: 90%

“…Several lines of evidence indicate that excitatory amino acids and GABA participate in the regulation of pituitary vasopressin release. Excitatory amino acids agonists stimulate vasopressin synthesizing cells, both in vitro ( 5–8) and in vivo ( 9, 10). It has been demonstrated that intracerebroventricular microinjection of GABA inhibits vasopressin release induced by hypertonic saline ( 11).…”

mentioning

confidence: 99%

The Effects of Ionotropic Agonists of Excitatory Amino Acids on the Release of Arginine Vasopressin in Rat Hypothalamic Slices

Joanny

Steinberg

Guerrero

et al. 2000

J Neuroendocrinology

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The effects of ionotropic excitatory amino acids agonists on the release of vasopressin from rat hypothalamic slices were studied. Incubation with increasing doses of NMDA, kainate or AMPA decreased the release of vasopressin in a dose-dependent manner. The values of the IC50 were 1.0, 9.6, or 3.7 x 10-8 M, respectively. The inhibitory effect of the various excitatory amino acids tested was blocked by coincubation with their respective antagonists. Vasopressin secretion was stimulated to 140.3 +/- 7.6% of controls when the slices were obtained from chronically (7 days) salt-loaded rats. Addition of 1 x 10-7 M NMDA or 1 x 10-6 M kainate to the incubation medium antagonized the salt loading-induced increase in vasopressin release. Incubation with 1 x 10-4 M tetrodotoxin did not change basal vasopressin release, but it blocked the decrease in vasopressin secretion induced by 1 x 10-7 M NMDA or 1 x 10-6 M kainate or 1 x 10-6 M AMPA. Incubation with 1 x 10-5 M phaclophen (a GABAB antagonist) and 1 x 10-5 M bicuculline (a GABAA antagonist) was without effect on basal vasopressin secretion while it reversed the inhibition of vasopressin release induced by 1 x 10-7 M NMDA. Incubation with 1 x 10-6 M GABA alone decreased vasopressin secretion to 64.6 +/- 6.9% of control values. The inhibitory effect of GABA did not change when 1 x 10-7 M NMDA was added to the incubation medium. These findings demonstrate that ionotropic excitatory amino acids agonists inhibit vasopressin secretion from hypothalamic slices. They strongly suggest that this inhibitory effect is mediated through local GABAergic interneurones.

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“…The release of VP and its excretion can be directly assessed in an in vivo rat antidiuretic bioassay Bisset & Fairhall, 1996). Muscarine chloride, a potent stimulator of VP release in this model, caused a profound but reversible antidiuretic response which was comparable in both normal and transgenic JP17 animals.…”

Section: Antidiuretic Bioassaymentioning

confidence: 98%

“…injections of muscarine chloride (20 ng) or by I.V. injections of sodium nitrosopentacyano (400 mg); these doses have previously been shown to release VP acutely in this preparation Bisset et al 1992;Bisset & Fairhall, 1996). Blood samples were withdrawn from the femoral arterial line via a threeway tap into heparinised tubes, and the plasma separated and frozen for subsequent RIA.…”

Section: Antidiuretic Bioassaymentioning

confidence: 99%

Transgenesis and neuroendocrine physiology: a transgenic rat model expressing growth hormone in vasopressin neurones

Wells¹,

Flavell²,

Bisset³

et al. 2003

The Journal of Physiology

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Human growth hormone (hGH) and bovine neurophysin (bNP) DNA reporter fragments were inserted into the rat vasopressin (VP) and oxytocin (OT) genes in a 44 kb cosmid construct used to generate two lines of transgenic rats, termed JP17 and JP59. Both lines showed specific hGH expression in magnocellular VP cells in the hypothalamic paraventricular (PVN) and supraoptic nuclei (SON). hGH was also expressed in parvocellular neurones in suprachiasmatic nuclei (SCN), medial amygdala and habenular nuclei in JP17 rats; the rat OT-bNP (rOT-bNP) transgene was not expressed in either line. Immunohistochemistry and radioimmunoassay showed hGH protein in the hypothalamus from where it was transported in varicose fibres via the median eminence to the posterior pituitary gland. Immunogold electron microscopy showed hGH co-stored with VP-NP in the same granules. The VP-hGH transgene did not affect water balance, VP storage or release in vivo. Drinking 2 % saline for 72 h increased hypothalamic transgene hGH mRNA expression, and depleted posterior pituitary hGH and VP stores in parallel. In anaesthetised, water-loaded JP17 rats, hGH was released with VP in response to an acute hypovolumic stimulus (sodium nitrosopentacyano, 400 microg I.V.). JP17 rats had a reduced growth rate, lower anterior pituitary rGH contents, and a reduced amplitude of endogenous pulsatile rGH secretion assessed by automated blood microsampling in conscious rats, consistent with a short-loop feedback of the VP-hGH on the endogenous GH axis. This transgenic rat model enables us to study physiological regulation of hypothalamic transgene protein production, transport and secretion, as well as its effects on other neuroendocrine systems in vivo.

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Release of vasopressin and oxytocin by excitatory amino acid agonists and the effect of antagonists on release by muscarine and hypertonic saline, in the rat in vivo

Cited by 13 publications

References 30 publications

Body Sodium Overload Modulates the Firing Rate and Fos Immunoreactivity of Serotonergic Cells of Dorsal Raphe Nucleus

Body Sodium Overload Modulates the Firing Rate and Fos Immunoreactivity of Serotonergic Cells of Dorsal Raphe Nucleus

The Effects of Ionotropic Agonists of Excitatory Amino Acids on the Release of Arginine Vasopressin in Rat Hypothalamic Slices

Transgenesis and neuroendocrine physiology: a transgenic rat model expressing growth hormone in vasopressin neurones

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