Regulation of Tracheal Ciliary Beat Frequency by Nitric Oxide Synthase Substrate L-Arginine

ORL ◽  
2010 ◽  
Vol 72 (1) ◽  
pp. 6-11 ◽  
Author(s):  
Jian Jiao ◽  
Demin Han ◽  
Na Meng ◽  
Shanzhe Jin ◽  
Luo Zhang
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Beat Frequency ◽  
Ciliary Beat Frequency ◽  
Oxide Synthase ◽  
Ciliary Beat

scholarly journals Expression of Endothelial Nitric Oxide Synthase in Ciliated Epithelia of Rats

2003 ◽  
Vol 51 (1) ◽  
pp. 81-87 ◽  
Author(s):  
Xinhua Zhan ◽  
Dechun Li ◽  
Roger A. Johns
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Endothelial Nitric Oxide Synthase ◽  
Vascular Tissue ◽  
Beat Frequency ◽  
Ciliary Beat Frequency ◽  
Cell Types ◽  
Ependymal Cells ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Endothelial nitric oxide synthase (eNOS), originally found in the endothelium of vascular tissue, also exists in other cell types, including ciliated epithelia of airways. The eNOS is ultrastructurally localized to the basal body of the microtubules of the cilia, and nitric oxide (NO) stimulates ciliary beat frequency (CBF). We examined whether the expression of eNOS is present in ciliated cells of other organs. Western blotting analysis revealed that eNOS was expressed in the rat cerebrum, lung, trachea, testis, and oviduct. Immunohistochemical staining showed that eNOS was localized in the ciliated epithelia of airways, oviduct, testis, and ependymal cells of brain in addition to the endothelium and smooth muscle of the vasculature. To confirm the activation of eNOS in the ciliated epithelia, we examined the effect of l-arginine (L-Arg), the substrate of NOS, on the production of nitrite and nitrate (NOx) in the cultured explants of rat trachea. l-Arg (100 μM) increased NOx levels significantly ( p<0.05). In explants exposed to inhibitors of NOS, the effect of l-Arg on the production of NOx was blocked. These findings suggest that epithelial NO plays an important role in signal transduction associated with ciliary functions.

Honorable Mention — Student Research Award 1995: Signal Transduction Mechanisms in Substance P-Mediated Ciliostimulation

1995 ◽  
Vol 113 (5) ◽  
pp. 582-588 ◽  
Author(s):  
Rodney J. Schlosser ◽  
Judith M. Czaja ◽  
Thomas V. McCaffrey
Keyword(s):  
Nitric Oxide ◽  
Substance P ◽  
Beat Frequency ◽  
Ciliary Beat Frequency ◽  
Ciliary Activity ◽  
Intermediate Step ◽  
Nitric Oxide Production ◽  
Oxide Production ◽  
Vitro Effect ◽  
Ciliary Beat

Substance P is a neuropeptide released by afferent neurons in the respiratory tract during inflammatory reactions. It produces effects on blood vessels, bronchial smooth muscle, nasal glands, and respiratory cilia. We studied the in vitro effect of substance P on the ciliary beat frequency of human adenoid explants and its mechanism of action. Substance P was added to cultured adenoid at concentrations of 10−10, 10−8, 10−6, and 10−4 mol/L. Ciliary beat frequency was determined with phase-contrast microscopy and microphotometry. Substance P increased ciliary beat frequency a maximum of 11.9% ± 3.8% ( p < 0.01). Diclofenac (10−6 mol/L) significantly blocked the ciliostimulatory effects of SP ( p < 0.022), indicating that prostaglandin synthesis is an intermediate step in the action of substance P on ciliary beat frequency. The L-arginine analogs, NG-nitro-L-arginine methyl ester and NG-monomethyl-L-arginine, inhibit nitric oxide synthesis from L-arginine. L-Arginine analogs (10−4 to 10−2 mol/L) inhibited the effect of substance P ( p < 0.02 at the higher concentration). This inhibition was reversed by adding L-arginine, demonstrating that nitric oxide production is a required step in substance P-induced ciliostimulation. Substance P stimulates ciliary activity in human nasal mucosa as a result of secondary production and release of endogenous prostaglandins and nitric oxide. It is likely that inflammatory disease processes that stimulate release of substance P and subsequent prostaglandin and nitric oxide production modify mucociliary transport. Pharmacologic modification of substance P and its second messengers may eventually permit regulation of this important defense mechanism and control of neurogenic inflammation.

scholarly journals Asymmetric Dimethylarginine Blocks Nitric Oxide-Mediated Alcohol-Stimulated Cilia Beating

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
T. A. Wyatt ◽  
S. M. Wells ◽  
Z. A. Alsaidi ◽  
J. M. DeVasure ◽  
E. B. Klein ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Epithelial Cells ◽  
Asymmetric Dimethylarginine ◽  
Beat Frequency ◽  
Alcohol Exposure ◽  
Bronchial Epithelial Cells ◽  
Mouse Lung ◽  
Bronchial Epithelial ◽  
Oxide Synthase

The airway epithelium is exposed to alcohol during drinking through direct exhalation of volatized ethanol from the bronchial circulation. Alcohol exposure leads to a rapid increase in the cilia beat frequency (CBF) of bronchial epithelial cells followed by a chronic desensitization of cilia stimulatory responses. This effect is governed in part by the nitric oxide regulation of cyclic guanosine and adenosine monophosphate-dependent protein kinases (PKG and PKA) and is not fully understood. Asymmetric dimethylarginine (ADMA), an endogenous inhibitor of nitric oxide synthase, is implicated in the pathogenesis of several pulmonary disorders. We hypothesized that the inhibition of nitric oxide synthase by ADMA blocks alcohol-stimulated increases in CBF. To test this hypothesis, ciliated primary bovine bronchial epithelial cells (BBEC) were preincubated with ADMA (100 µM) and stimulated with 100 mM ethanol. CBF was measured and PKA assayed. By 1 hr, ethanol activated PKA, resulting in elevated CBF. Both alcohol-induced PKA activation and CBF were inhibited in the presence of ADMA. ADMA alone had no effect on PKA activity or CBF. Using a mouse model overexpressing the ADMA-degrading enzyme, dimethylarginine dimethylaminohydrolase (DDAH), we examined PKA and CBF in precision-cut mouse lung slices. Alcohol-stimulated increases in lung slice PKA and CBF were temporally enhanced in the DDAH mice versus control mice.

Nitric oxide levels and ciliary beat frequency in indigenous New Zealand children

2005 ◽  
Vol 39 (3) ◽  
pp. 238-246 ◽  
Author(s):  
E.A. Edwards ◽  
C. Douglas ◽  
S. Broome ◽  
J. Kolbe ◽  
C.G. Jensen ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
New Zealand ◽  
Beat Frequency ◽  
Ciliary Beat Frequency ◽  
Ciliary Beat

Ethanol stimulates apparent nitric oxide-dependent ciliary beat frequency in bovine airway epithelial cells

1995 ◽  
Vol 268 (4) ◽  
pp. L596-L600 ◽  
Author(s):  
J. H. Sisson
Keyword(s):  
Nitric Oxide ◽  
Epithelial Cells ◽  
Airway Epithelium ◽  
Beat Frequency ◽  
Primary Cultures ◽  
Ciliary Beat Frequency ◽  
Airway Epithelial Cells ◽  
Ethanol Ingestion ◽  
Ciliary Motility ◽  
Ciliary Beat

The mucociliary apparatus of the lung provides an important host-defense function by clearing the upper airway of inhaled particles and infectious microorganisms. Because lung host defenses are impaired in alcoholics, we hypothesized that ethanol would decrease ciliary motility in airway epithelium. Ciliary beat frequency (CBF) was measured by videomicroscopy in primary cultures of ciliated bovine bronchial epithelial cells (BBECs). Ethanol rapidly stimulated ciliary motility in a time-dependent fashion with concentrations as low as 10 mM. No detectable decreases in ciliary motility were noted until ethanol concentrations exceeded 1,000 mM. Because many substances stimulate ciliary motility by releasing nitric oxide (NO) via upregulation of nitric oxide synthase (NOS), we preincubated ciliated BBECs with a stereospecific NOS inhibitor, NG-monomethyl-L-arginine (L-NMMA). L-NMMA completely blocked ethanol-induced stimulation of CBF, which could be subsequently restored by adding either L-arginine or sodium nitroprusside, which is a direct NO donor. These results indicate that ethanol, at clinically relevant concentrations, stimulates the release of NO by airway epithelium that upregulates ciliary motility. The rapidity of this response suggests upregulation of the constitutive NOS, known to be present in airway epithelium, and may explain the increases in mucociliary clearance observed in previous studies of ethanol ingestion in animals and in humans. These data also suggest a novel signal transduction pathway, the NO/NOS system, by which ethanol may exert some of its diverse biologic effects.

Modulation of Airway Epithelial Cell Ciliary Beat Frequency by Nitric Oxide

1993 ◽  
Vol 191 (1) ◽  
pp. 83-88 ◽  
Author(s):  
B. Jain ◽  
I. Rubinstein ◽  
R.A. Robbins ◽  
K.L. Leise ◽  
J.H. Sisson
Keyword(s):  
Nitric Oxide ◽  
Epithelial Cell ◽  
Airway Epithelial Cell ◽  
Beat Frequency ◽  
Ciliary Beat Frequency ◽  
Airway Epithelial ◽  
Ciliary Beat
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