scholarly journals Vasopressin Autoreceptors and Nitric Oxide-Dependent Glutamate Release Are Required for Somatodendritic Vasopressin Release from Rat Magnocellular Neuroendocrine Cells Responding to Osmotic Stimuli

Endocrinology ◽  
2007 ◽  
Vol 148 (2) ◽  
pp. 479-489 ◽  
Author(s):  
E. R. Gillard ◽  
C. G. Coburn ◽  
A. de Leon ◽  
E. P. Snissarenko ◽  
L. G. Bauce ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Glutamate Release ◽  
Neuroendocrine Cells ◽  
Vasopressin Release ◽  
Magnocellular Neuroendocrine Cells ◽  
Osmotic Stimuli

Nitric oxide modulates synaptic glutamate release during anoxia

1997 ◽  
Vol 228 (1) ◽  
pp. 50-54 ◽  
Author(s):  
Alexander N Katchman ◽  
Norman Hershkowitz
Keyword(s):  
Nitric Oxide ◽  
Glutamate Release

Abstract P322: Vasopressin Release is Enhanced Before the Development of Preeclampsia in Humans Despite Exaggerated Suppression of Plasma Osmolality

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Mark K Santillan ◽  
Sabrina M Scroggins ◽  
Alyssa T Ray ◽  
Phillip C Witcher ◽  
Jeremy A Sandgren ◽  
...  
Keyword(s):  
Pregnant Women ◽  
Gestational Age ◽  
Clinical Symptoms ◽  
Freezing Point ◽  
Tissue Bank ◽  
Plasma Osmolality ◽  
Fetal Tissue ◽  
Chronic Hypertension ◽  
Vasopressin Release ◽  
Osmotic Stimuli

Plasma osmolality (Osm) suppression is of critical importance to maintain appropriate blood volume to perfuse the uterus during pregnancy. Osm is reduced starting at the fifth week of gestation via increased arginine vasopressin (AVP) secretion. This increased secretion is maintained via a decrease in the AVP/osmotic release threshold. We previously demonstrated that pregnant women who develop preeclampsia (PreE) exhibit exaggerated AVP secretion as early as the 6th week of gestation via measurement of copeptin, the stable C-terminal fragment of AVP. It is unclear whether AVP secretion is elevated before the onset of PreE due to osmotic or non-osmotic stimuli. We tested the hypothesis that elevated AVP secretion before PreE may be associated with elevated Osm (a strong stimulant of AVP secretion). Plasma and clinical data from pregnant women were obtained from the University of Iowa Maternal-Fetal Tissue Bank (IRB#200910784). Osm was measured using the freezing-point suppression technique. Osm was assessed in non-pregnant women (n=109), pregnant women who later developed PreE (n=12 for 7-12 weeks, n=9 for 16-24 weeks), and maternal and gestational age matched controls (n=25 for 6-13 weeks, n=15 for 14-27 weeks). As expected, Osm was decreased in control pregnancies (non-pregnant 291±1 vs pregnant 286±1 mOsm/kg, p<0.05). Contrary to our hypothesis, the Osm decrease was exaggerated in women who would later develop PreE (1st trimester: PreE 279±4 vs control 287±3, and 2 nd trimester: PreE 277±4 vs control 285±3 mOsm/kg; effect of PreE p<0.05, gestational age p=NS, interaction p=NS) even after controlling for age, BMI, diabetes, chronic hypertension, history of preeclampsia, and gravida (model p<0.05). Despite suppressed Osm, plasma copeptin was elevated in the PreE group at all timepoints (p<0.05). These data support the conclusion that long before the development of clinical symptoms of PreE, the rate of secretion of AVP is inappropriately increased despite maintenance of normal osmotic-regulating actions of AVP. This effect must be the result of increased non-osmotic stimuli for AVP, and a suppression of the AVP/osmotic release threshold beyond that observed in control pregnancies.

Increased Expression of Cyclooxygenase and Nitric Oxide Isoforms, and Exaggerated Sensitivity to Prostaglandin E2, in the Rat Lumbar Spinal Cord 3 Days after L5–L6 Spinal Nerve Ligation

2006 ◽  
Vol 104 (2) ◽  
pp. 328-337 ◽  
Author(s):  
Darren D. O’Rielly ◽  
Christopher W. Loomis
Keyword(s):  
Nitric Oxide ◽  
Spinal Cord ◽  
Neuropathic Pain ◽  
Glutamate Release ◽  
Spinal Nerve ◽  
Spinal Nerve Ligation ◽  
Withdrawal Threshold ◽  
Enhanced Sensitivity ◽  
Sham Surgery ◽  
Inducible Nos

Background Spinal prostaglandins seem to be important in the early pathogenesis of experimental neuropathic pain. Here, the authors investigated changes in the expression of cyclooxygenase and nitric oxide synthase (NOS) isoforms in the lumbar, thoracic, and cervical spinal cord and the pharmacologic sensitivity to spinal prostaglandin E2 (PGE2) after L5-L6 spinal nerve ligation (SNL). Methods Male Sprague-Dawley rats, fitted with intrathecal catheters, underwent SNL or sham surgery 3 days before experimentation. Paw withdrawal threshold was monitored for up to 20 days. Immunoblotting, spinal glutamate release, and behavioral testing were examined 3 days after SNL. Results Allodynia (paw withdrawal threshold &lt; or = 4 g) was evident 1 day after SNL and remained stable for 20 days. Paw withdrawal threshold was unchanged (P &gt; 0.05) from baseline (&gt; 15 g) after sham surgery except for a small but significant decrease on day 20. Cyclooxygenase 2, neuronal NOS, and inducible NOS were significantly increased in the ipsilateral lumbar dorsal horn after SNL. Expression in the contralateral dorsal horn and ventral horns (lumbar segments) or bilaterally (thoracic and cervical segments) was unchanged from sham controls. This was accompanied by a significant decrease in both the EC50 of PGE2-evoked glutamate release and the ED50 of PGE2 on brush-evoked allodynia. Enhanced sensitivity to PGE2 was localized to lumbar segments of SNL animals and attenuated by SC-51322 or S(+)-ibuprofen, but not R(-)-ibuprofen (100 mum). Conclusion The increased expression of cyclooxygense-2, neuronal NOS, and inducible NOS and the enhanced sensitivity to PGE2 in spinal segments affected by SNL support the hypothesis that spinal prostanoids play an early pathogenic role in experimental neuropathic pain.

scholarly journals Nitric Oxide and the Neuroendocrine Control of the Osmotic Stress Response in Teleosts

2019 ◽  
Vol 20 (3) ◽  
pp. 489 ◽  
Author(s):  
Carla Cioni ◽  
Elisa Angiulli ◽  
Mattia Toni
Keyword(s):  
Nitric Oxide ◽  
Stress Response ◽  
Osmotic Stress ◽  
No Synthase ◽  
Hormone Release ◽  
Neurosecretory Neurons ◽  
Osmotic Stress Response ◽  
Osmotic Challenge ◽  
Osmotic Stimuli

The involvement of nitric oxide (NO) in the modulation of teleost osmoresponsive circuits is suggested by the facts that NO synthase enzymes are expressed in the neurosecretory systems and may be regulated by osmotic stimuli. The present paper is an overview on the research suggesting a role for NO in the central modulation of hormone release in the hypothalamo-neurohypophysial and the caudal neurosecretory systems of teleosts during the osmotic stress response. Active NOS enzymes are constitutively expressed by the magnocellular and parvocellular hypophysiotropic neurons and the caudal neurosecretory neurons of teleosts. Moreover, their expression may be regulated in response to the osmotic challenge. Available data suggests that the regulatory role of NO appeared early during vertebrate phylogeny and the neuroendocrine modulation by NO is conservative. Nonetheless, NO seems to have opposite effects in fish compared to mammals. Indeed, NO exerts excitatory effects on the electrical activity of the caudal neurosecretory neurons, influencing the amount of peptides released from the urophysis, while it inhibits hormone release from the magnocellular neurons in mammals.

Two nitridergic peptides are encoded by the gene capability in Drosophila melanogaster

2002 ◽  
Vol 282 (5) ◽  
pp. R1297-R1307 ◽  
Author(s):  
Laura Kean ◽  
William Cazenave ◽  
Laurence Costes ◽  
Kate E. Broderick ◽  
Shirley Graham ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Renal Tubule ◽  
Fluid Secretion ◽  
Neuroendocrine Cells ◽  
The Other ◽  
Pheromone Biosynthesis ◽  
Nitric Oxide Production ◽  
Intracellular Ca ◽  
Fluid Production ◽  
Secretion Rates

A Drosophila gene ( capability, capa) at 99D on chromosome 3R potentially encodes three neuropeptides: GANMGLYAFPRV-amide (capa-1), ASGLVAFPRV-amide (capa-2), and TGPSASSGLWGPRL-amide (capa-3). Capa-1 and capa-2 are related to the lepidopteran hormone cardioacceleratory peptide 2b, while capa-3 is a novel member of the pheromone biosynthesis-activating neuropeptide/diapause hormone/pyrokinin family. By immunocytochemistry, we identified four pairs of neuroendocrine cells likely to release the capa peptides into the hemolymph: one pair in the subesophageal ganglion and the other three in the abdominal neuromeres. In the Malpighian (renal) tubule, capa-1 and capa-2 increase fluid secretion rates, stimulate nitric oxide production, and elevate intracellular Ca2+ and cGMP in principal cells. Capa-stimulated fluid secretion, but not intracellular Ca2+ concentration rise, is inhibited by the guanylate cyclase inhibitor methylene blue. The actions of capa-1 and capa-2 are not synergistic, implying that both act on the same pathways in tubules. The capa gene is thus the first to be shown to encode neuropeptides that act on renal fluid production through nitric oxide.

P033. Nitric oxide mediates cytokine-induced enhancement of calcium-dependent glutamate release from astrocytes

Nitric Oxide ◽  
2006 ◽  
Vol 14 (4) ◽  
pp. 29
Author(s):  
Tomoaki Ida ◽  
Shigeru Tsunoda ◽  
Masayuki Hara ◽  
Shunji Kozaki ◽  
Hideshi Ihara
Keyword(s):  
Nitric Oxide ◽  
Glutamate Release ◽  
Calcium Dependent
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