Stimulation of Glyceraldehyde-3-Phosphate Dehydrogenase mRNA Levels by Endogenous Nitric Oxide in Cytokine-Activated Endothelium

1995 ◽  
Vol 217 (1) ◽  
pp. 363-369 ◽  
Author(s):  
J. Bereta ◽  
M. Bereta
Keyword(s):  
Nitric Oxide ◽  
Mrna Levels ◽  
Endogenous Nitric Oxide ◽  
Stimulation Of

The Effect of Endogenous Nitric Oxide on Cholinergic Ciliary Stimulation of Human Nasal Mucosa

2004 ◽  
Vol 114 (9) ◽  
pp. 1642-1647 ◽  
Author(s):  
J??rgen Alberty ◽  
Christian August ◽  
Wolfgang Stoll ◽  
Claudia Rudack
Keyword(s):  
Nitric Oxide ◽  
Nasal Mucosa ◽  
Human Nasal Mucosa ◽  
Endogenous Nitric Oxide ◽  
Stimulation Of

5-Hydroxytryptamine-induced NO-dependent relaxation in isolated strips of monkey popliteal lymph nodes

1995 ◽  
Vol 268 (6) ◽  
pp. H2246-H2251
Author(s):  
R. Mizuno ◽  
T. Ohhashi
Keyword(s):  
Nitric Oxide ◽  
Lymph Node ◽  
Lymph Nodes ◽  
The Other ◽  
Plot Analysis ◽  
Basal Tone ◽  
Endogenous Nitric Oxide ◽  
Popliteal Lymph Nodes ◽  
Ics 205 930 ◽  
Stimulation Of

5-Hydroxytryptamine (5-HT, 0.01-100 microM) and 5-carboxamidotryptamine (5-CT, 0.001-10 microM) produced dose-related relaxations in strips cut from monkey popliteal lymph nodes precontracted with a perfusion of Krebs bicarbonate solution containing 80 mM KCl. These 5-HT agonists caused no significant effect on the basal tone of the lymph node strips. The 5-HT-induced relaxation is competitively antagonized by pretreatment with a selective 5-HT1-like receptor antagonist, methiothepin (0.01-0.1 microM). Schild plot analysis showed that the pA2 value and slope of methiothepin against 5-HT were 8.80 +/- 0.11 and 0.99 +/- 0.07 (n = 6), respectively. Pretreatment with methysergide (0.01-0.1 microM) significantly attenuated the 5-HT-induced relaxation of the strips. On the other hand, treatment with ketanserin (0.01-0.1 microM) and ICS-205-930 (0.01-0.1 microM) caused no significant effect on the 5-HT-or the 5-CT-induced relaxation. The 5-HT-induced relaxation was significantly reduced by 10 microM NG-monomethyl-L-arginine, which was reversed by 1 mM L-arginine. The relaxation in the lymph node strips was also significantly reduced by treatment with 10 microM methylene blue but not with 30 microM aspirin. These results suggest that 5-HT1-like receptors exist in the monkey popliteal lymph nodes. Stimulation of these receptors produces an endogenous nitric oxide (NO)-dependent relaxation in lymph node smooth muscle through an activation of cytosolic guanylate cyclase in the cells.

Stimulation of endogenous nitric oxide production is involved in the inhibitory effect of adrenomedullin on aldosterone secretion in the rat

Peptides ◽  
2001 ◽  
Vol 22 (6) ◽  
pp. 923-926 ◽  
Author(s):  
Piera Rebuffat ◽  
Ludwik K Malendowicz ◽  
Gastone G Nussdorfer ◽  
Giuseppina Mazzocchi
Keyword(s):  
Nitric Oxide ◽  
Inhibitory Effect ◽  
Nitric Oxide Production ◽  
Aldosterone Secretion ◽  
Oxide Production ◽  
Endogenous Nitric Oxide ◽  
Stimulation Of

Interaction of endogenous nitric oxide and CGRP in sensory neuron-induced gastric vasodilation

1995 ◽  
Vol 268 (5) ◽  
pp. G791-G796 ◽  
Author(s):  
R. Y. Chen ◽  
P. H. Guth
Keyword(s):  
Nitric Oxide ◽  
Sensory Nerves ◽  
Cgrp Receptor ◽  
Synthesis Inhibitor ◽  
Calcitonin Gene ◽  
Endogenous Nitric Oxide ◽  
Cgrp Receptor Antagonist ◽  
Dose Dependent ◽  
Stimulation Of

Stimulation of capsaicin-sensitive sensory nerves induces gastric mucosal hyperemia, which is mediated in part by both calcitonin gene-related peptide (CGRP) and nitric oxide (NO). In the present study, we used in vivo microscopy in anesthetized rats to determine 1) whether these agents were released locally at the submucosal level and, if so, 2) whether CGRP dilates arterioles via release of endothelium-derived NO. Intragastric capsaicin (160 microM) dilated submucosal arterioles from 25 +/- 3 to 67 +/- 8 microns. The intragastric capsaicin-induced vasodilation was markedly reversed not only by intravenous administration of the NO synthesis inhibitor NG-nitro-L-arginine methyl ester (L-NAME) but also by submucosal suffusion of either L-NAME or the CGRP receptor antagonist human CGRP-(8-37). The latter findings indicate that both NO and CGRP are released locally at the submucosal level. Submucosal application of CGRP induced dose-dependent dilation of gastric submucosal arterioles, which was significantly attenuated by L-NAME. However, at the same degree of vasodilation (42 microns), the dilation induced with submucosal CGRP was much less attenuated by NO synthesis inhibition (-28%) compared with that induced with intragastric capsaicin (-79%). This indicates that endothelium-derived NO released by CGRP was not the only source of submucosal NO in the latter response. There must be another as yet undetermined source of submucosal NO, e.g., possibly nitroxidergic nerves.

Glutamate stimulation of acetylcholine release from myenteric plexus is mediated by endogenous nitric oxide

2005 ◽  
Vol 66 (3) ◽  
pp. 229-234 ◽  
Author(s):  
Elisaveta A. Milusheva ◽  
Vjara I. Kuneva ◽  
Dimitar E. Itzev ◽  
Nadejda I. Kortezova ◽  
Beata Sperlagh ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Myenteric Plexus ◽  
Acetylcholine Release ◽  
Endogenous Nitric Oxide ◽  
Stimulation Of

Basal nitric oxide production curtails arteriolar vasoconstrictor responses to ANG II in rat kidney

1996 ◽  
Vol 271 (2) ◽  
pp. F365-F373 ◽  
Author(s):  
H. Ikenaga ◽  
R. W. Fallet ◽  
P. K. Carmines
Keyword(s):  
Nitric Oxide ◽  
Rat Kidney ◽  
No Synthase ◽  
Ang Ii ◽  
Juxtamedullary Nephron ◽  
Endogenous Nitric Oxide ◽  
Synthase Inhibitor ◽  
Baseline Diameter ◽  
Stimulation Of

Experiments were performed to test the hypothesis that renal arteriolar vasoconstrictor responses to angiotensin II (ANG II) are curtailed through a mechanism that involves stimulation of endogenous nitric oxide (NO) synthesis. The in vitro blood-perfused juxtamedullary nephron technique was exploited to monitor arteriolar lumen diameter responses to exogenous ANG II before and during treatment with the NO synthase inhibitor N omega-nitro-L-arginine (L-NNA). Under control conditions, 1 nM ANG II reduced afferent and efferent arteriolar diameters by 13 and 11%, respectively. In the presence of L-NNA, 1 nM ANG II decreased afferent diameter by 26% and efferent diameter by 35%. This augmentation could not be attributed to the L-NNA-induced decrease in baseline diameter. L-NNA also augmented vasopressin responses, indicating a lack of agonist specificity in this interaction. ANG II reactivity during L-NNA treatment was not enhanced when tissue NO activity was fixed at basal levels (exposure to 1 microM sodium nitroprusside). These results indicate that endogenous NO modulates the vasoconstrictive impact of ANG II on both afferent and efferent arterioles of juxtamedullary nephrons and that this process does not require stimulation of NO synthesis.

Interleukin-10 Stimulation of Endogenous Nitric Oxide Release from Human Saphenous Veins Diminishes Immunocyte Adherence

1997 ◽  
Vol 30 (1) ◽  
pp. 90-95 ◽  
Author(s):  
George B. Stefano ◽  
V. Brix Christensen ◽  
Else Tonnesen ◽  
Yu Liu ◽  
Thomas K. Hughes ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Interleukin 10 ◽  
Nitric Oxide Release ◽  
Saphenous Veins ◽  
Endogenous Nitric Oxide ◽  
Stimulation Of

Inducible nitric oxide synthase subserves cholinergic vasodilation in retina

2005 ◽  
Vol 22 (3) ◽  
pp. 371-377 ◽  
Author(s):  
ALEJANDRO BERRA ◽  
SABRINA GANZINELLI ◽  
MARIO SARAVIA ◽  
ENRI BORDA ◽  
LEONOR STERIN-BORDA
Keyword(s):  
Gene Expression ◽  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Retinal Vessel ◽  
Inos Mrna ◽  
Mrna Levels ◽  
Mrna Gene ◽  
Oxide Synthase ◽  
Mrna Gene Expression ◽  
Stimulation Of

In this paper, we investigate the role of muscarinic acetylcholine receptor (mAChR) activity in the regulation of inducible (i) nitric oxide synthase (iNOS) expression and activity. The signaling pathway involved is also examined. These experiments also provide a link between mAChR activation and the nitric oxide (NO)-dependent regulation of retinal vascular diameter. The diameter of the retinal vessels at a distance of 1 disc diameter from the center of the optic disc was measured in rats using digital retinal photography, and both iNOS-mRNA gene expression and NOS were specifically measured using RT-PCR and [U-14C] citrulline assays, respectively. Stimulation of M1 and M3 mAChR with carbachol caused an increase in vessel diameter, in iNOS-mRNA levels and in NOS activity in the retina. Aminoguanidine, an inhibitor of iNOS, attenuated all these effects. Inhibitors of phospholipase C (PLC) and protein kinase C (PKC) but not calcium/calmodulin (CaM) prevented the muscarinic-dependent increase in iNOS-mRNA levels. The results obtained suggest that the activation of mAChR increases retinal vessel diameters by increasing the production of nitric oxide (NO) through iNOS activation and iNOS-mRNA gene expression. The mechanism appears to occur secondarily to stimulation of PLC and PKC enzymatic activity.

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