EFFECTS OF Β-Adrenoceptor STIMULANTS ON THE CANINE TRACHEAL CILIATED CELLS

Yanaura, Saiζo; Imamura, Naoto; Misawa, Miwa

doi:10.1016/s0021-5198(19)52770-6

Cited by 4 publications

(3 citation statements)

References 16 publications

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“…Sympathetic reflexes have effects on mucociliary activity in vivo, because electrical stimulation of the sympathetic nerves is known to increase mucociliary activity, 17 probably through stimulation of β 2 -receptors. [18][19][20] The findings of this investigation, in which propranolol pretreatment produced a fall in mucociliary activity, suggest sympathetic nervous modulation of ciliary function. However, in previous studies at our laboratory we failed to find an inhibitory effect of propranolol on the mucociliary system in the rabbit maxillary sinus.…”

Section: Otolaryngology-head and Neck Surgerymentioning

confidence: 66%

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

Runer

Cervin

Lindberg

et al. 1998

Otolaryngol.--head neck surg.

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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(-3) mol/L, and this effect was reversibly blocked by pretreatment with the NO synthase (NOS) inhibitor N(G)-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 microg/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 beta-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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Section: Otolaryngology-head and Neck Surgerymentioning

confidence: 66%

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

Runer

Cervin

Lindberg

et al. 1998

Otolaryngol.--head neck surg.

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“…Cyclic AMP has been shown to activate or increase the beat frequency of cilia and flagella [22], but most of the studies on the regulation of ciliary activity by cyclic nucleotides have been on unicellular eukaryotes. There have been two reports on the stimulatory effect of cAMP analogues on CBF in canine (5] and rabbit (27] trachea. There appear to be no published papers on the effe.…”

Section: Pathways Controlling Cbfmentioning

confidence: 99%

“…Neurohormones and neurotransmitters associated with the autonomic nervous system have a significant influence on mucociliary activity [3]. It has l;>een demonstrated in vitro that adrenergic drugs cause an increase in CBF in both animal [4][5][6][7] and human [8] tissues. Recent in vivo studies on dogs confirm the role of autonomic agonists in regulating CBF [9) .…”

mentioning

confidence: 99%

Effect of cyclic AMP on ciliary activity of human respiratory epithelium

Benedetto¹,

Manara-Shediac²,

Mehta³

1991

Eur Respir J

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In order to investigate the effect of cyclic adenosine monophosphate (cAMP) on ciliary beat frequency (CBF) in human respiratory epithelium, cells were brushed from the inferior nasal turbinates of three groups of ten subjects: awake adults (aged 20-34 yrs), anaesthetized children (2-15 yrs) and anaesthetized adults (19-61 yrs). Cells from the awake adults were also studied after storage for 24 h in tissue culture medium. CBF was measured in vitro with a photometric technique at room temperature (22.0 +/- 1.5 degrees C). Samples were mounted in a perfusion chamber and challenged with either control solutions, dibutyryl cAMP (10(-4) or 10(-3) M), or the cyclic nucleotide-dependent protein kinase inhibitor 1-(5-isoquinolinylsulphonyl)-2-methylpiperazine (H-7). Dibutyryl cAMP (10(-3) M) caused a significant increase in CBF in all groups studied: awake adults (+1.1 Hz; p less than 0.01), anaesthetized children (+1.2 Hz; p less than 0.01), anaesthetized adults (+1.2 Hz; p less than 0.01), stored cells (+1.1 Hz; p less than 0.01). This response was inhibited by preincubation with H-7 (10(-4) and 10(-3) M). It is concluded that cAMP is a regulator of ciliary activity in human respiratory epithelium.

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