scholarly journals Resting Tension Affects eNOS Activity in a Calcium-Dependent Way in Airways

2007 ◽  
Vol 2007 ◽  
pp. 1-6 ◽  
Author(s):  
Eudoxia Kitsiopoulou ◽  
Apostolia A. Hatziefthimiou ◽  
Konstantinos I. Gourgoulianis ◽  
Paschalis-Adam Molyvdas
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscle ◽  
Calcium Concentration ◽  
Kinase Inhibitors ◽  
Calcium Dependent ◽  
Enos Activity ◽  
Resting Tension ◽  
Smooth Muscle Contractions ◽  
Oxide Synthase ◽  
Inducible Nos

The alteration of resting tension (RT) from 0.5 g to 2.5 g increased significantly airway smooth muscle contractions induced by acetylcholine (ACh) in rabbit trachea. The decrease in extracellular calcium concentration[Ca2+]ofrom 2 mM to 0.2 mM reduced ACh-induced contractions only at 2.5 g RT with no effect at 0.5 g RT. The nonselective inhibitor of nitric oxide synthase (NOS),NG-nitro-L-arginine methyl ester (L-NAME) increased ACh-induced contractions at 2.5 g RT. The inhibitor of inducible NOS, S-methylsothiourea or neuronal NOS, 7-nitroindazole had no effect. At 2.5 g RT, the reduction of[Ca2+]ofrom 2 mM to 0.2 mM abolished the effect of L-NAME on ACh-induced contractions. The NO precursor L-arginine or the tyrosine kinase inhibitors erbstatin A and genistein had no effect on ACh-induced contractions obtained at 2.5 g RT. Our results suggest that in airways, RT affects ACh-induced contractions by modulating the activity of epithelial NOS in a calcium-dependent, tyrosine-phosphorylation-independent way.

Estrogen Does Not Induce the Calcium-Dependent Nitric Oxide Synthase in Cultured Human Uterine Endothelial and Myometrial Smooth Muscle Cells

1997 ◽  
Vol 34 (4) ◽  
pp. 281-288 ◽  
Author(s):  
Walter Tschugguel ◽  
Zydi Zhegu ◽  
Christian Schneeberger ◽  
Eva Tantscher ◽  
Klaus Czerwenka ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscle ◽  
Nitric Oxide Synthase ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Calcium Dependent ◽  
Oxide Synthase

scholarly journals Nitric oxide synthase is induced in sporulation of Physarum polycephalum

2001 ◽  
Vol 15 (10) ◽  
pp. 1299-1309
Author(s):  
Georg Golderer ◽  
Ernst R. Werner ◽  
Stefan Leitner ◽  
Peter Gröbner ◽  
Gabriele Werner-Felmayer
Keyword(s):  
Nitric Oxide ◽  
Physarum Polycephalum ◽  
Light Exposure ◽  
Amino Acid Identity ◽  
Specific Gene ◽  
Starvation Period ◽  
Binding Motifs ◽  
Calcium Dependent ◽  
Oxide Synthase ◽  
Inducible Nos

The myxomycete Physarum polycephalum expresses a calcium-independent nitric oxide (NO) synthase (NOS) resembling the inducible NOS isoenzyme in mammals. We have now cloned and sequenced this, the first nonanimal NOS to be identified, showing that it shares < 39% amino acid identity with known NOSs but contains conserved binding motifs for all NOS cofactors. It lacks the sequence insert responsible for calcium dependence in the calcium-dependent NOS isoenzymes. NOS expression was strongly up-regulated inPhysarum macroplasmodia during the 5-day starvation period needed to induce sporulation competence. Induction of both NOS and sporulation competence were inhibited by glucose, a growth signal and known repressor of sporulation, and byl-N6–(1-iminoethyl)-lysine (NIL), an inhibitor of inducible NOS. Sporulation, which is triggered after the starvation period by light exposure, was also prevented by 1H-[1,2,4]oxadiazolo-[4,3-a]quinoxalin-1-one (ODQ), an inhibitor of NO-sensitive guanylate cyclase. In addition, also expression oflig1, a sporulation-specific gene, was strongly attenuated by NIL or ODQ. 8-Bromo-cGMP, added 2 h before the light exposure, restored the capacity of NIL-treated macroplasmodia to express lig1 and to sporulate. This indicates that the second messenger used for NO signaling in sporulation of Physarum is cGMP and links this signaling pathway to expression of lig1.

Thrombin Prevents the Expression of Inducible Nitric Oxide Synthase in Vascular Smooth Muscle Cells by a Proteolytically-Activated Thrombin Receptor

1995 ◽  
Vol 74 (03) ◽  
pp. 980-986 ◽  
Author(s):  
Valérie B Schini-Kerth ◽  
Beate Fißithaler ◽  
Thomas T Andersen ◽  
John W Fenton ◽  
Paul M Vanhoutte ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Inducible Nitric Oxide Synthase ◽  
Muscle Cells ◽  
Thrombin Receptor ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

SummaryProteolytically active forms of thrombin (α- and γ-thrombin) and thrombin receptor peptides inhibited the release of nitrite, a stable endproduct of nitric oxide, evoked by interleukin-1 β(IL-1 β) in cultured vascular smooth muscle cells while proteolytically inactive forms [D-Phe-Pro-Arg chloromethyl ketone-α-thrombin (PPACK-α- thrombin) and diisopropylphosphoryl-α-thrombin (DIP-α-thrombin)] had either no or only minimal inhibitory effects. Under bioassay conditions, perfusates from columns containing IL-1 β-activated vascular smooth muscle cells or cells treated with IL-1βplus PPACK-α-thrombin relaxed detector blood vessels. These relaxations were abolished by the inhibitor of nitric oxide synthesis, NG-nitro-L arginine. No relaxations were obtained with untreated cells or IL-1 β-treated cells in the presence of α-thrombin. The expression of inducible nitric oxide synthase mRNA and protein in vascular smooth muscle cells by IL-1 β was impaired by α-thrombin. These results demonstrate that thrombin regulates the expression of the inducible nitric oxide synthase at a transcriptional level via the proteolytic activation of the thrombin receptor in vascular smooth muscle cells

HALOTHANE INHIBITS INTERLEUKIN-1 β-STIMULATED INDUCTION OF NITRIC OXIDE SYNTHASE IN VASCULAR SMOOTH MUSCLE

1994 ◽  
Vol 81 (SUPPLEMENT) ◽  
pp. A681
Author(s):  
H. Maeda ◽  
M. Yamamoto ◽  
K. Mizumoto ◽  
T. Yosbiyama ◽  
Y. Hatano
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscle ◽  
Nitric Oxide Synthase ◽  
Vascular Smooth Muscle ◽  
Interleukin 1 ◽  
Oxide Synthase

Nitric oxide synthase inhibitors 7- and 6-nitroindazole relax smooth muscle in vitro

1994 ◽  
Vol 256 (1) ◽  
pp. R5-R6 ◽  
Author(s):  
Andrew D. Medhurst ◽  
Carol Greenlees ◽  
Andrew A. Parsons ◽  
Susan J. Smith
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscle ◽  
Nitric Oxide Synthase ◽  
Nitric Oxide Synthase Inhibitors ◽  
Oxide Synthase

scholarly journals Analysis of NOS Gene Polymorphisms in Relation to Cluster Headache and Predisposing Factors in Sweden

2020 ◽  
Vol 11 (1) ◽  
pp. 34
Author(s):  
Caroline Ran ◽  
Julia M. Michalska ◽  
Carmen Fourier ◽  
Christina Sjöstrand ◽  
Elisabet Waldenlind ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cluster Headache ◽  
Genetic Variants ◽  
Potential Candidate ◽  
Nitric Oxide Signaling ◽  
Minor Alleles ◽  
Oxide Synthase ◽  
Trigeminal Reflex ◽  
Inducible Nos ◽  
Nos Gene

Cluster headache is characterized by activation of the autonomic-trigeminal reflex. Nitric oxide can trigger headaches in patients, and nitric oxide signaling is known to be affected in cluster headache. Based on the hypothesis of nitric oxide being involved in cluster headache pathophysiology we investigated nitric oxide synthases as potential candidate genes for cluster headache. We analyzed eight variants in the three forms of nitric oxide synthase (NOS) genes, inducible NOS (iNOS), endothelial NOS (eNOS) and neuronal NOS (nNOS), and tested for association with cluster headache. Swedish cluster headache patients (n = 542) and controls (n = 581) were genotyped using TaqMan® assays on an Applied Biosystems 7500 qPCR cycler. This is the largest performed genetic study on NOS involvement in cluster headache so far. We found an association between cluster headache and one iNOS haplotype consisting of the minor alleles of rs2297518 and rs2779249 (p = 0.022). In addition, one of the analyzed nNOS variants, rs2682826, was associated with reported triptan use (p = 0.039). Our data suggest that genetic variants in NOS genes do not have a strong influence on cluster headache pathophysiology, but that certain combinations of genetic variants in NOS genes may influence the risk of developing the disorder or triptan use.

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