scholarly journals The Mechanism of Ciliary Stimulation by Acetylcholine

2002 ◽  
Vol 119 (4) ◽  
pp. 329-339 ◽  
Author(s):  
Orna Zagoory ◽  
Alex Braiman ◽  
Zvi Priel
Keyword(s):  
Muscarinic Receptors ◽  
Guanylate Cyclase ◽  
Beat Frequency ◽  
Ciliary Beat Frequency ◽  
Time Dependent ◽  
Camp Signaling ◽  
Second Phase ◽  
Independent Manner ◽  
Molecular Events ◽  
Stimulation Of

Stimulation of ciliary cells through muscarinic receptors leads to a strong biphasic enhancement of ciliary beat frequency (CBF). The main goal of this work is to delineate the chain of molecular events that lead to the enhancement of CBF induced by acetylcholine (ACh). Here we show that the Ca2+, cGMP, and cAMP signaling pathways are intimately interconnected in the process of cholinergic ciliary stimulation. ACh induces profound time-dependent increase in cGMP and cAMP concentrations mediated by the calcium–calmodulin complex. The initial strong CBF enhancement in response to ACh is mainly governed by PKG and elevated calcium. The second phase of CBF enhancement induced by ACh, a stable moderately elevated CBF, is mainly regulated by PKA in a Ca2+-independent manner. Inhibition of either guanylate cyclase or of PKG partially attenuates the response to ACh of [Ca2+]i, but completely abolishes the response of CBF. Inhibition of PKA moderately attenuates and significantly shortens the responses to ACh of both [Ca2+]i and CBF. In addition, PKA facilitates the elevation in [Ca2+]i and cGMP levels induced by ACh, whereas an unimpeded PKG activity is essential for CBF enhancement mediated by either Ca2+ or PKA.

scholarly journals Role of calcium and calmodulin in ciliary stimulation induced by acetylcholine

2001 ◽  
Vol 280 (1) ◽  
pp. C100-C109 ◽  
Author(s):  
Orna Zagoory ◽  
Alex Braiman ◽  
Larisa Gheber ◽  
Zvi Priel
Keyword(s):  
Phospholipase C ◽  
Muscarinic Receptors ◽  
Elevated Level ◽  
Beat Frequency ◽  
Ciliary Beat Frequency ◽  
Combined Effect ◽  
Molecular Events ◽  
Intracellular Ca ◽  
Stimulation Of

The goal of this work was to elucidate the molecular events underlying stimulation of ciliary beat frequency (CBF) induced by acetylcholine (ACh) in frog esophagus epithelium. ACh induces a profound increase in CBF and in intracellular Ca2+ concentration ([Ca2+]i) through M1 and M3 muscarinic receptors. The [Ca2+]i slowly decays to the basal level, while CBF stabilizes at an elevated level. These results suggest that ACh triggers Ca2+-correlated and -uncorrelated modes of ciliary stimulation. ACh response is abolished by the phospholipase C (PLC) inhibitor U-73122 and by depletion of intracellular Ca2+ stores but is unaffected by reduction of extracellular Ca2+ concentration and by blockers of Ca2+influx. Therefore, ACh activates PLC and mobilizes Ca2+solely from intracellular stores. The calmodulin inhibitors W-7 and calmidazolium attenuate the ACh-induced increase in [Ca2+]i but completely abolish the elevation in CBF. Therefore, elevation of [Ca2+]i is necessary for CBF enhancement but does not lead directly to it. The combined effect of Ca2+ elevation and of additional factors, presumably mobilized by Ca2+-calmodulin, results in a robust CBF enhancement.

Capsaicin-activated bronchial- and alveolar-initiated pathways regulating tracheal ciliary beat frequency

1994 ◽  
Vol 77 (3) ◽  
pp. 1239-1245 ◽  
Author(s):  
M. Eljamal ◽  
L. B. Wong ◽  
D. B. Yeates
Keyword(s):  
Low Dose ◽  
Beat Frequency ◽  
Ciliary Beat Frequency ◽  
Neural Stimulation ◽  
Short Exposure ◽  
Tracheal Lumen ◽  
Prolonged Stimulation ◽  
Prior Administration ◽  
Stimulation Of ◽  
Ciliary Beat

We questioned whether the prolonged stimulation of ciliary beat frequency (CBF) to a short exposure of low-dose capsaicin (Wong et al. J. Appl. Physiol. 68: 257–2580, 1990) could be due to the activation of indirect pathways involving neural reflexes initiated independently in the bronchi and alveoli. Tracheal CBF (CBFtr) was measured temporally in anesthetized groups of 10 dogs by means of heterodyne-mode correlation analysis laser light scattering. To elucidate the site of the afferent neural stimulation and the efferent mediators affecting the ciliated epithelium, capsaicin (3 nM) aerosol was delivered for 4 min, either predominantly to the bronchi or to the alveolar regions, with use of pulsed aerosol techniques. This resulted in 13 pg of bronchial (85%) and 10 pg of alveolar (96%) capsaicin deposited, which caused marked stimulation of CBFtr with maxima at 7 and 35 min, respectively. Prior administration of aerosolized indomethacin to the bronchi or aerosolized cromolyn to the alveoli inhibited the bronchial and alveolar responses, respectively. Prior administration of aerosolized hexamethonium to the tracheal lumen blocked the stimulatory CBFtr responses from both capsaicin challenges. Ipratropium or propranolol aerosols delivered to the tracheal lumen also inhibited these responses. It is proposed that these pathways comprise one set of sensitive mechanisms to ensure a prolonged stimulation of CBF to effect the removal of secretions and the irritant from the lungs.

Regulation of ciliary beat frequency by autonomic mechanisms: in vitro

1988 ◽  
Vol 65 (4) ◽  
pp. 1895-1901 ◽  
Author(s):  
L. B. Wong ◽  
I. F. Miller ◽  
D. B. Yeates
Keyword(s):  
Laser Light ◽  
Beat Frequency ◽  
Ciliary Beat Frequency ◽  
Atropine Sulfate ◽  
Adrenergic Agonist ◽  
Muscarinic Cholinergic ◽  
Autonomic Receptors ◽  
Stimulation Of ◽  
Ciliary Beat

The ciliated epithelium of the mammalian trachea separates the neurohumoral milieu of the tissue from that of the environment of the airway lumen. To determine whether specific autonomic receptors regulating ciliary beat frequency (CBF) were located on mucosal or serosal sides, we measured CBF by heterodyne mode correlation analysis laser light scattering in bovine tracheal tissues mounted in a two-sided chamber. A beta 2-adrenergic agonist, fenoterol, at 10(-7) M, stimulated serosal CBF from 7.9 +/- 1.3 to 20.2 +/- 5.8 Hz (P less than 0.01) and mucosal CBF from 6.6 +/- 0.9 to 14.7 +/- 4.6 Hz (P less than 0.01). A muscarinic cholinergic agonist, methacholine, at 10(-7) M, increased mucosal CBF from 8.4 +/- 1.0 to 19.5 +/- 5.5 Hz (P less than 0.01) and serosal CBF from 8.0 +/- 0.9 to 15.4 +/- 5.0 Hz (P less than 0.01). The differences in stimulation of CBF on the mucosal and serosal sides between fenoterol and methacholine were significant (P less than 0.01). Studies in which these autonomic agonist stimulating effects were inhibited by their respective antagonists, propranolol and atropine sulfate, demonstrated that CBF can be regulated independently by mediators both in the submucosa and within the mucus lining.

Time-dependent changes in nasal ciliary beat frequency

2010 ◽  
Vol 267 (9) ◽  
pp. 1383-1387 ◽  
Author(s):  
J. Ulrich Sommer ◽  
Shalini Gross ◽  
Karl Hörmann ◽  
Boris A. Stuck
Keyword(s):  
Beat Frequency ◽  
Ciliary Beat Frequency ◽  
Time Dependent ◽  
Ciliary Beat

scholarly journals PKA induces Ca2+ release and enhances ciliary beat frequency in a Ca2+-dependent and -independent manner

1998 ◽  
Vol 275 (3) ◽  
pp. C790-C797 ◽  
Author(s):  
Alex Braiman ◽  
Orna Zagoory ◽  
Zvi Priel
Keyword(s):  
Beat Frequency ◽  
Ciliary Beat Frequency ◽  
Ciliary Activity ◽  
Experimental Conditions ◽  
Independent Manner ◽  
Ciliary Beating ◽  
Independent Mechanism ◽  
Intracellular Ca ◽  
Ciliary Beat

The intent of this work was to evaluate the role of cAMP in regulation of ciliary activity in frog mucociliary epithelium and to examine the possibility of cross talk between the cAMP- and Ca2+-dependent pathways in that regulation. Forskolin and dibutyryl cAMP induced strong transient intracellular Ca2+ concentration ([Ca2+]i) elevation and strong ciliary beat frequency enhancement with prolonged stabilization at an elevated plateau. The response was not affected by reduction of extracellular Ca2+concentration. The elevation in [Ca2+]iwas canceled by pretreatment with 1,2-bis(2-aminophenoxy)ethane- N, N, N′, N′-tetraacetic acid-AM, thapsigargin, and a phospholipase C inhibitor, U-73122. Under those experimental conditions, forskolin raised the beat frequency to a moderately elevated plateau, whereas the initial strong rise in frequency was completely abolished. All effects were canceled by H-89, a selective protein kinase A (PKA) inhibitor. The results suggest a dual role for PKA in ciliary regulation. PKA releases Ca2+ from intracellular stores, strongly activating ciliary beating, and, concurrently, produces moderate prolonged enhancement of the beat frequency by a Ca2+-independent mechanism.

scholarly journals TRP Channels as Sensors of Bacterial Endotoxins

Toxins ◽  
2018 ◽  
Vol 10 (8) ◽  
pp. 326 ◽  
Author(s):  
Brett Boonen ◽  
Yeranddy Alpizar ◽  
Victor Meseguer ◽  
Karel Talavera
Keyword(s):  
Transient Receptor Potential ◽  
Trp Channels ◽  
Inflammatory Responses ◽  
Beat Frequency ◽  
Receptor Potential ◽  
Ciliary Beat Frequency ◽  
Airway Epithelial Cells ◽  
Independent Manner ◽  
Genetic Ablation ◽  
Bacterial Endotoxins

The cellular and systemic effects induced by bacterial lipopolysaccharides (LPS) have been solely attributed to the activation of the Toll-like receptor 4 (TLR4) signalling cascade. However, recent studies have shown that LPS activates several members of the Transient Receptor Potential (TRP) family of cation channels. Indeed, LPS induces activation of the broadly-tuned chemosensor TRPA1 in sensory neurons in a TLR4-independent manner, and genetic ablation of this channel reduced mouse pain and inflammatory responses triggered by LPS and the gustatory-mediated avoidance to LPS in fruit flies. LPS was also shown to activate TRPV4 channels in airway epithelial cells, an effect leading to an immediate production of bactericidal nitric oxide and to an increase in ciliary beat frequency. In this review, we discuss the role of TRP channels as sensors of bacterial endotoxins, and therefore, as crucial players in the timely detection of invading gram-negative bacteria.

Stimulation of tracheal ciliary beat frequency by capsaicin

1990 ◽  
Vol 68 (6) ◽  
pp. 2574-2580 ◽  
Author(s):  
L. B. Wong ◽  
I. F. Miller ◽  
D. B. Yeates
Keyword(s):  
Ipratropium Bromide ◽  
Laser Light ◽  
Beat Frequency ◽  
Ciliary Beat Frequency ◽  
Base Line ◽  
Aerosol Delivery ◽  
Temporal Response ◽  
Stimulation Of ◽  
Ciliary Beat

To determine the possible involvement of neural and cyclooxygenase pathways whereby irritants might affect cilia activity in vivo, the temporal response of canine tracheal ciliary beat frequency (CBF) to the inhaled surrogate irritant capsaicin was studied. CBF was measured on the ventral midtracheal surface of barbiturate-anesthetized eucapnically ventilated beagle dogs by heterodyne-mode laser light scattering. After base-line CBF was established, hexamethonium bromide (2 mg/kg iv), ipratropium bromide (0.5 microgram/kg iv), indomethacin (2 mg/kg iv), or intravenous 0.9% saline was administered. Aerosolized 3 Z 10(-9) M capsaicin in 0.9% saline was delivered for 2 min, and CBF was measured for the following 60 min. Control experiments used 0.9% saline sham aerosol with a 0.9% saline sham block. Aerosolized capsaicin stimulated CBF from a base line of 6.2 +/- 1.4 (SD) Hz (n = 230) to a mean maximum of 17.7 +/- 7.3 Hz (n = 16) 23 min after aerosol delivery, and CBF returned to base line within 60 min. Neither hexamethonium bromide, ipratropium bromide, nor indomethacin changed CBF from base-line values. The episodic CBF stimulatory response to capsaicin after commencement of aerosol was completely inhibited by hexamethonium bromide. Ipratropium bromide partially inhibited the first 15 min and totally inhibited the following 45 min of stimulatory response. Indomethacin inhibited the initial 15 min but had less effect on the following 45 min of stimulatory response. These data indicate that multiple stimulatory mechanisms function over a prolonged period of time to affect the removal of irritants from the airways and that these mechanisms differ from those involved in the maintenance of basal CBF.

Role of NO generation in beta-adrenoceptor-mediated stimulation of rabbit airway ciliary motility

1995 ◽  
Vol 268 (6) ◽  
pp. C1342-C1347 ◽  
Author(s):  
J. Tamaoki ◽  
A. Chiyotani ◽  
M. Kondo ◽  
K. Konno
Keyword(s):  
Methyl Ester ◽  
Epithelial Cells ◽  
Beat Frequency ◽  
Ciliary Beat Frequency ◽  
Stimulatory Action ◽  
Maximal Increase ◽  
Ciliary Motility ◽  
Beta Adrenoceptor ◽  
Stimulation Of

To determine possible contribution of nitric oxide (NO) to the stimulatory action of beta-adrenoceptor agonist on ciliary motility, we measured ciliary beat frequency (CBF) of rabbit cultured tracheal epithelial cells by photoelectric method and NO release by specific amperometric sensors for this molecule in vitro. Salbutamol increased CBF, an effect that was potentiated by superoxide dismutase. Pretreatment of cells with NG-nitro-L-arginine methyl ester (L-NAME) attenuated the salbutamol-induced increase in CBF, causing a rightward displacement of the concentration-response curve by 2-2.5 log units, whereas NG-nitro-D-arginine methyl ester had no effect. The inhibitory effect of L-NAME was reversed by L-arginine but not by D-arginine. Immersion of the NO-selective electrode in the medium containing epithelial cells detected baseline current of 4.6-14.5 pA, which was abolished by L-NAME. Salbutamol dose-dependently increased the concentration of NO in the medium, the maximal increase being 56.2 +/- 5.3 nM (mean +/- SE; P < 0.001). These results suggest that NO is spontaneously released by airway epithelium and that the enhanced release of this molecule may play a role in the beta-adrenoceptor-mediated stimulation of ciliary motility

KINETICS OF OXYGEN INDUCED STIMULATION OF CILIARY BEAT FREQUENCY

1989 ◽  
Vol 71 (Supplement) ◽  
pp. A1109
Author(s):  
R. A. Harrison ◽  
L. B. Hong ◽  
D. B. Yeates
Keyword(s):  
Beat Frequency ◽  
Ciliary Beat Frequency ◽  
Kinetics Of ◽  
Stimulation Of ◽  
Ciliary Beat
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