scholarly journals Detection of nitric oxide synthase (NOS) in somatostatin-producing cells of human and murine stomach and pancreas.

1996 ◽  
Vol 44 (4) ◽  
pp. 339-346 ◽  
Author(s):  
M A Burrell ◽  
L M Montuenga ◽  
M García ◽  
A C Villaro
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Ganglion Cells ◽  
Secretory Granules ◽  
The Body ◽  
Gastric Epithelium ◽  
Thin Sections ◽  
Immunocytochemical Techniques ◽  
D Cells ◽  
Oxide Synthase

The aim of this study was to identify by immunocytochemistry the distribution of nitric oxide synthase (NOS) in human and murine gastric epithelium. Using two different antisera specific for neuronal NOS (nNOS), we detected nNOS immunoreactivity in endocrine cells of the epithelium of the body and pyloric regions as well as in ganglion cells of the intrinsic plexi of the stomach of the three species studied. Both immunocytochemistry of contiguous sections and double immunolabeling methods showed that the nNOS-immunoreactive cells were also immunoreactive for somatostatin. Co-localization of nNOS and somatostatin has also been found in the pancreatic islets, where strong nNOS immunoreactivity appeared in scattered cells, which were peripheral in rat and mouse islets and more randomly distributed in human. The possibility of crossreactivity between the antisera against nNOS and somatostatin was ruled out by means of absorption controls. Immunocytochemical techniques were also applied to thin sections, confirming the immunostaining of gastric D-cells, which was restricted principally to the secretory granules. The possible functional implications of these findings for gastric and pancreatic physiology are discussed.

Loss of Retinal Ganglion Cells Following Retinal Ischemia: The Role of Inducible Nitric Oxide Synthase

2002 ◽  
Vol 75 (5) ◽  
pp. 521-528 ◽  
Author(s):  
Arthur H. Neufeld ◽  
Shin-ichiro Kawai ◽  
Sucharita Das ◽  
Smita Vora ◽  
Elizabeth Gachie ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Retinal Ganglion Cells ◽  
Inducible Nitric Oxide Synthase ◽  
Ganglion Cells ◽  
Retinal Ischemia ◽  
Retinal Ganglion ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

Nitric oxide synthase is an active enzyme in the spiral ganglion cells of the rat cochlea

1994 ◽  
Vol 79 (1-2) ◽  
pp. 39-47 ◽  
Author(s):  
Carlton J. Zdanski ◽  
Jiri Prazma ◽  
Peter Petrusz ◽  
Gail Grossman ◽  
Eileen Raynor ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Ganglion Cells ◽  
Spiral Ganglion ◽  
Active Enzyme ◽  
Rat Cochlea ◽  
Oxide Synthase

Helicobacter pylori enhances an expression of inducible nitric oxide synthase (iNOS) in human gastric epithelium

2001 ◽  
Vol 120 (5) ◽  
pp. A653-A654
Author(s):  
Qunsheng Song ◽  
Marilyn Owens ◽  
Duane T. Smoot ◽  
Hassan Ashktorab ◽  
Benjamin D. Gold
Keyword(s):  
Nitric Oxide ◽  
Helicobacter Pylori ◽  
Nitric Oxide Synthase ◽  
Inducible Nitric Oxide Synthase ◽  
Gastric Epithelium ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

Neuronal nitric oxide synthase is expressed in the axotomized ganglion cells of the rat retina

2003 ◽  
Vol 986 (1-2) ◽  
pp. 174-180 ◽  
Author(s):  
Eun-Jin Lee ◽  
Keun-Young Kim ◽  
Tae-Hyung Gu ◽  
Jung-Il Moon ◽  
In-Beom Kim ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Ganglion Cells ◽  
Neuronal Nitric Oxide Synthase ◽  
Rat Retina ◽  
Oxide Synthase

In situ localization of nitric oxide synthase and direct evidence of NO production in rat retinal ganglion cells

2002 ◽  
Vol 933 (2) ◽  
pp. 118-129 ◽  
Author(s):  
Yuichi Tsumamoto ◽  
Keisuke Yamashita ◽  
Masaya Takumida ◽  
Koji Okada ◽  
Satoshi Mukai ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Retinal Ganglion Cells ◽  
Direct Evidence ◽  
Ganglion Cells ◽  
No Production ◽  
Retinal Ganglion ◽  
Oxide Synthase

scholarly journals Possible Origins and Distribution of Immunoreactive Nitric Oxide Synthase-Containing Nerve Fibers in Cerebral Arteries

1993 ◽  
Vol 13 (1) ◽  
pp. 70-79 ◽  
Author(s):  
Kazuhiko Nozaki ◽  
Michael A. Moskowitz ◽  
Kenneth I. Maynard ◽  
Naoki Koketsu ◽  
Ted M. Dawson ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Ganglion Cells ◽  
Cerebral Arteries ◽  
Nerve Fibers ◽  
Circle Of Willis ◽  
Sphenopalatine Ganglion ◽  
Sprague Dawley ◽  
Pial Arteries ◽  
Oxide Synthase

The distribution of perivascular nerve fibers expressing nitric oxide synthase (NOS)-immunoreactivity was examined in Sprague–Dawley and Long–Evans rats using affinity-purified rabbit antisera raised against NOS from rat cerebellum. NOS immunoreactivity was expressed within the endothelium and adventitial nerve fibers in both rat strains. Labeled axons were abundant and dense in the proximal anterior and middle cerebral arteries, but were less numerous in the caudal circle of Willis and in small pial arteries. The sphenopalatine ganglia were the major source of positive fibers in these vessels. Sectioning postganglionic parasympathetic fibers from both sphenopalatine ganglia reduced the density of NOS-immunoreactive (IR) nerve fibers by >75% in the rostral circle of Willis. Moreover, NOS-IR was present in 70–80% of sphenopalatine ganglion cells. Twenty percent of these neurons also contained vasoactive intestinal polypeptide (VlP)-immunoreactivity. By contrast, the superior cervical ganglia did not contain NOS-IR cells. In the trigeminal ganglion, NO-IR neurons were found chiefly within the ophthalmic division; ∼10–15% of neurons were positively labeled. Colocalization with calcitonin gene-related peptide (CGRP) was not observed. Sectioning the major trigeminal branch innervating the circle of Willis decreased positive fibers by ≤25% in the ipsilateral vessels. In the nodose ganglion, 20–30% of neurons contained NOS-immunoreactivity, whereas less than 1% were in the C2 and C3 dorsal root ganglia. Three human circles of Willis obtained at autopsy showed sparse immunoreactive fibers, chiefly within vessels of the posterior circulation. Postmortem delay accounted for some of the reduced density. Our findings indicate that nerve fibers innervating cerebral arteries may serve as a nonendothelial source of the vasodilator nitric oxide (NO). The coexistence of NOS and VIP within sphenopalatine ganglion cells raises the possibility that two vasodilatory agents, one, a highly diffusable short-lived, low-molecular-weight molecule, and the other, a polar 28 amino acid-containing peptide, may serve as coneuromediators within the cerebral circulation.

scholarly journals The sensitivity of light-evoked responses of retinal ganglion cells is decreased in nitric oxide synthase gene knockout mice

2007 ◽  
Vol 7 (14) ◽  
pp. 7 ◽  
Author(s):  
Guo-Yong Wang ◽  
Deborah A. van der List ◽  
Joseph P. Nemargut ◽  
Julie L. Coombs ◽  
Leo M. Chalupa
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Retinal Ganglion Cells ◽  
Knockout Mice ◽  
Ganglion Cells ◽  
Gene Knockout ◽  
Evoked Responses ◽  
Retinal Ganglion ◽  
Gene Knockout Mice ◽  
Oxide Synthase

scholarly journals Beneficial Effect of a Multistrain Synbiotic Prodefen® Plus on the Systemic and Vascular Alterations Associated with Metabolic Syndrome in Rats: The Role of the Neuronal Nitric Oxide Synthase and Protein Kinase A

Nutrients ◽  
2020 ◽  
Vol 12 (1) ◽  
pp. 117 ◽  
Author(s):  
Pablo Llévenes ◽  
Raquel Rodrigues-Díez ◽  
Laia Cros-Brunsó ◽  
Mᵃ Isabel Prieto ◽  
Laura Casaní ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Metabolic Syndrome ◽  
Body Weight ◽  
Protein Kinase ◽  
Nitric Oxide Synthase ◽  
Protein Kinase A ◽  
Neuronal Nitric Oxide Synthase ◽  
The Body ◽  
Oxide Synthase ◽  
Kinase A

A high fat diet (HFD) intake is crucial for the development and progression of metabolic syndrome (MtS). Increasing evidence links gut dysbiosis with the metabolic and vascular alterations associated with MtS. Here we studied the use of a combination of various probiotic strains together with a prebiotic (synbiotic) in a commercially available Prodefen® Plus. MtS was induced by HFD (45%) in male Wistar rats. Half of the MtS animals received Prodefen® Plus for 4 weeks. At 12 weeks, we observed an increase in body weight, together with the presence of insulin resistance, liver steatosis, hypertriglyceridemia and hypertension in MtS rats. Prodefen® Plus supplementation did not affect the body weight gain but ameliorated all the MtS-related symptoms. Moreover, the hypertension induced by HFD is caused by a diminished both nitric oxide (NO) functional role and release probably due to a diminished neuronal nitric oxide synthase (nNOS) activation by protein kinase A (PKA) pathway. Prodefen® Plus supplementation for 4 weeks recovered the NO function and release and the systolic blood pressure was returned to normotensive values as a result. Overall, supplementation with Prodefen® Plus could be considered an interesting non-pharmacological approach in MtS.

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