scholarly journals Nitric oxide modulates peristaltic muscle activity associated with fluid circulation in the sea pansy Renilla koellikeri

2005 ◽  
Vol 208 (10) ◽  
pp. 2005-2017 ◽  
Author(s):  
M. Anctil
Keyword(s):  
Nitric Oxide ◽  
Muscle Activity ◽  
Fluid Circulation ◽  
Renilla Koellikeri

LPS-induced muscularis macrophage nitric oxide suppresses rat jejunal circular muscle activity

1999 ◽  
Vol 277 (2) ◽  
pp. G478-G486 ◽  
Author(s):  
Mark K. Eskandari ◽  
Jörg C. Kalff ◽  
Timothy R. Billiar ◽  
Kenneth K. W. Lee ◽  
Anthony J. Bauer
Keyword(s):  
Nitric Oxide ◽  
Muscle Activity ◽  
Contractile Activity ◽  
Circular Muscle ◽  
Fold Increase ◽  
Inos Mrna ◽  
Organ Bath ◽  
Cellular Mechanisms ◽  
Circular Smooth Muscle

Cellular mechanisms of sepsis-induced ileus remain an enigma. The study aim was to determine the role of nitric oxide (NO) in mediating the suppression of rat jejunal circular smooth muscle activity during endotoxemia. Isolated muscularis inducible NO synthase (iNOS) mRNA was measured by RT-PCR, immunohistochemistry was employed to localize iNOS protein, and contractile activity was measured in an organ bath. The low basal expression of muscularis iNOS mRNA expression was increased in a time-dependent fashion after lipopolysaccharide (LPS), resulting in a 20-fold increase over controls 3 h after injection. Immunohistochemistry of muscularis whole mounts and dissociated muscularis cells for iNOS revealed staining only in the muscularis macrophages 12 h after LPS. LPS caused a 68% reduction in spontaneous muscle activity 12 h after injection, which improved by 53% after the in vitro application of the selective iNOS inhibitorl- N6-(1-iminoethyl)lysine. Similar results were obtained in C57BL/6 mice but not in iNOS knockout mice. These data demonstrate that macrophage iNOS plays an important role in mediating LPS-induced intestinal circular muscle suppression.

scholarly journals Effect of nitric oxide synthase inhibitors on ovum transport and oviductal smooth muscle activity in the rat oviduct

Reproduction ◽  
2000 ◽  
Vol 118 (1) ◽  
pp. 111-117 ◽  
Author(s):  
S Perez Martinez ◽  
M Viggiano ◽  
A. Franchi ◽  
M. Herrero ◽  
M. Ortiz ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscle ◽  
Nitric Oxide Synthase ◽  
Muscle Activity ◽  
Nitric Oxide Synthase Inhibitors ◽  
Ovum Transport ◽  
Oxide Synthase

Abstract 665: Endothelial Nitric Oxide Negatively Modulates Phenylephrine-induced Contraction In Matrix Metalloproteinase 2 (mmp-2)-filled Rabbit Aortic Rings

Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
Alejandro F Prado ◽  
Laena Pernomian ◽  
Lusiane M Bendhack ◽  
Raquel F Gerlach
Keyword(s):  
Nitric Oxide ◽  
Matrix Metalloproteinase ◽  
Muscle Activity ◽  
Vascular Function ◽  
Vascular Reactivity ◽  
Selective Inhibitor ◽  
Matrix Metalloproteinase 2 ◽  
Maximum Effect ◽  
Endothelial Nitric Oxide

Endothelial nitric oxide negatively modulates Phenylephrine-induced contraction in Matrix metalloproteinase 2 (MMP-2)-filled rabbit aortic rings The present study aimed to evaluate the vascular function of aortic rings after intraluminal injection of matrix metalloproteinase 2 (MMP-2) and contribution of endothelial nitric oxide (NO) in this response. METHODS: thoracic aorta isolated from New Zealand rabbits (3.0 Kg) was isolated and were performed in situ gelatinolytic assay (intraluminal exposure with Krebs solution or MMP-2 1.2 μg/mL, at 37° C for 30 minutes, with measure of fluorescence intensity - FI) or vascular reactivity. Cumulative concentration-effect curves for phenylephrine (PE, 0.1 nM - 10 μM/L) were performed in endothelium-intact (E+) or denuded (E-) aortic rings, in the absence or presence of L-NAME (non-selective inhibitor of NOS, 100 μM) or Hydroxycobalamine (scavenger of intracellular NO), 30 min before the PE curves on E+ rings. The vascular contraction was normalized by grams of tension by dry tissue (g/g) and were analyzed the agonist maximum effect (Emax) and potency (pD2). Data represent mean ± S.E.M and the results were statistically analyzed using Student t test, one-way or two-way ANOVA with Bonferroni pos-hoc (p<0,05). Results: In situ gelatinolytic activity was increased in the vessels filled with MMP-2 (19.19+0.93U,n=5) compared to vehicle (10.75+0.45U,n=5). In the vascular reactivity, E- aortic rings filled with MMP-2 increased Emax of PE (1893,28+122,40g/g,n=9) versus vehicle E- (1485.73+76.82g/g,n=9), but no differences were observed on Emax of E+ aortic rings (vehicle: 1416.13+120.87g/g,n=7; MMP-2: 1893.28+122.40g/g,n=9). The presence of L-NAME induced an increase in Emax of E+ aortic rings filled with vehicle (1817.60+76.37g/g,n=7) or MMP-2 (2340.50+130.43g/g,n=5). Hydroxycobalamine also increased the Emax of E+ aortic rings with vehicle (1889,81+129,17,n=6) or MMP-2 (2480,12+192,57,n=5). No difference of pD2 value was observed in this study. Conclusion: Data suggest this protease cross the aorta layers from the lumen. An increased vasoconstriction in E- vessels suggests a vascular smooth muscle activity of MMP-2. In the presence of L-NAME and Hydroxycobalamine, vessels filled with MMP-2 shows a greater maximum effect suggesting that NO exerts a negative modulation of the PE-induced vasoconstriction on MMP-2 aortic rings.

Modulation of smooth muscle activity by nitric oxide in the human upper urinary tract

1995 ◽  
Vol 23 (6) ◽  
pp. 391-394 ◽  
Author(s):  
H. H. Iversen ◽  
I. Ehr�n ◽  
L. E. Gustafsson ◽  
J. Adolfsson ◽  
N. P. Wiklund
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscle ◽  
Urinary Tract ◽  
Muscle Activity ◽  
Upper Urinary Tract

Localization of endothelial nitric oxide synthase in the normal and failing human atrial myocardium

1996 ◽  
Vol 54 ◽  
pp. 786-787
Author(s):  
Chi-Ming Wei ◽  
Margarita Bracamonte ◽  
Shi-Wen Jiang ◽  
Richard C. Daly ◽  
Christopher G.A. McGregor ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Heart Failure ◽  
Nitric Oxide Synthase ◽  
Endothelial Nitric Oxide Synthase ◽  
Cardiac Tissues ◽  
Mammalian Tissues ◽  
End Stage Heart Failure ◽  
End Stage ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Nitric oxide (NO) is a potent endothelium-derived relaxing factor which also may modulate cardiomyocyte inotropism and growth via increasing cGMP. While endothelial nitric oxide synthase (eNOS) isoforms have been detected in non-human mammalian tissues, expression and localization of eNOS in the normal and failing human myocardium are poorly defined. Therefore, the present study was designed to investigate eNOS in human cardiac tissues in the presence and absence of congestive heart failure (CHF).Normal and failing atrial tissue were obtained from six cardiac donors and six end-stage heart failure patients undergoing primary cardiac transplantation. ENOS protein expression and localization was investigated utilizing Western blot analysis and immunohistochemical staining with the polyclonal rabbit antibody to eNOS (Transduction Laboratories, Lexington, Kentucky).

Nitric Oxide Reduces Pressor Responsiveness During Ovine Hypoadrenocorticism

2001 ◽  
Vol 28 (5-6) ◽  
pp. 459-462
Author(s):  
Pini Orbach ◽  
Charles E Wood ◽  
Maureen Keller-Wood
Keyword(s):  
Nitric Oxide

Nitric oxide synthase and cellac disease

2001 ◽  
Vol 120 (5) ◽  
pp. A684-A684
Author(s):  
I DANIELS ◽  
I MURRAY ◽  
W GODDARD ◽  
R LONG
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Oxide Synthase
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