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

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.

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

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

Nitric Oxide is a Regulator of Mucociliary Activity in the Upper Respiratory Tract

1998 ◽  
Vol 119 (3) ◽  
pp. 278-287 ◽  
Author(s):  
Eugene N. Myers ◽  
Thomas Runer ◽  
Anders Cervin ◽  
Sven Lindberg ◽  
Rolf Uddman
Keyword(s):  
Nitric Oxide ◽  
Beat Frequency ◽  
Ciliary Beat Frequency ◽  
Sphenopalatine Ganglion ◽  
No Donor ◽  
Peak Response ◽  
Sinus Mucosa ◽  
Ciliary Beat

The in vitro effects of the nitric oxide (NO) substrate L-arginine on ciliary beat frequency and the in vivo effects of the NO donor sodium nitroprusside (SNP) on mucociliary activity were investigated in the rabbit maxillary sinus mucosa with photoelectric techniques. L-Arginine increased ciliary beat frequency in vitro with a maximum response of 27.1% ± 6.4% at 10-3mol/L, and this effect was reversibly blocked by pretreatment with the NO synthase (NOS) inhibitor NG-nitro-L-arginine, whereas D-arginine had no such effect. SNP increased mucociliary activity in vivo, the peak response of 36.8% ± 4.2% being obtained at the dose of 30.0 μg/kg. No tachyphylaxis was observed after repeat challenge with SNP. The increase in mucociliary activity caused by SNP was largely unaffected by pretreatment with the calcium channel blocker nifedipine, the cyclooxygenase inhibitor diclofenac, and the cholinergic antagonist atropine. The nonselective β-blocker propranolol delayed the peak response of SNP to 7 to 8 minutes after challenge, compared with 1 to 2 minutes after challenge in animals without pretreatment. The results show the NO substrate L-arginine and the NO donor SNP to have ciliostimulatory effects in vitro and in vivo, respectively. The occurrence of NOS production in the sphenopalatine ganglion and sinus mucosa of the rabbit was studied by immunohistochemistry for NOS activity or nicotinamide adenine dinucleotide phosphate-diaphorase histochemistry. The latter is an indirect sign of neuronal NOS activity. Numerous NOS-containing cell bodies were seen in the sphenopalatine ganglion; in the sinus mucosa a moderate supply of thin NOS-immunoreactive nerve fibers was seen. Taken together, the morphologic findings and the functional results indicate NO to be a regulator of mucociliary activity in upper airways.

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