-
Je něco špatně v tomto záznamu ?
The Prospect for Potent Sodium Voltage-Gated Channel Blockers to Relieve an Excessive Cough
M. Brozmanova, N. Pavelkova
Jazyk angličtina Země Česko
Typ dokumentu časopisecké články, přehledy
NLK
Directory of Open Access Journals
od 1991
Free Medical Journals
od 1998
PubMed Central
od 2020
ProQuest Central
od 2005-01-01
Medline Complete (EBSCOhost)
od 2006-01-01
Nursing & Allied Health Database (ProQuest)
od 2005-01-01
Health & Medicine (ProQuest)
od 2005-01-01
ROAD: Directory of Open Access Scholarly Resources
od 1998
- MeSH
- akční potenciály účinky léků fyziologie MeSH
- antitusika farmakologie terapeutické užití MeSH
- blokátory sodíkových kanálů řízených napětím farmakologie terapeutické užití MeSH
- kašel farmakoterapie patofyziologie MeSH
- lidé MeSH
- nociceptory účinky léků metabolismus MeSH
- sodíkové kanálky řízené napětím fyziologie MeSH
- zvířata MeSH
- Check Tag
- lidé MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- přehledy MeSH
An excessive, irritable, productive or non-productive coughing associated with airway inflammation belongs to pathological cough. Increased activation of airway vagal nociceptors in pathological conditions results from dysregulation of the neural pathway that controls cough. A variety of mediators associated with airway inflammation overstimulate these vagal airway fibers including C-fibers leading to hypersensitivity and hyperreactivity. Because current antitussives have limited efficacy and unwanted side effects there is a continual demand for the development of a novel more effective antitussives for a new efficacious and safe cough treatment. Therefore, inhibiting the activity of these vagal C-fibers represents a rational approach to the development of effective antitussive drugs. This may be achieved by blocking inflammatory mediator receptors or by blocking the generator potential associated with the specific ion channels. Because voltage-gated sodium channels (NaVs) are absolutely required for action potentials initiation and conduction irrespective of the stimulus, NaVs become a promising neural target. There is evidence that NaV1.7, 1.8 and 1.9 subtypes are predominantly expressed in airway cough-triggering nerves. The advantage of blocking these NaVs is suppressing C-fiber irrespective to stimuli, but the disadvantage is that by suppressing the nerves is may also block beneficial sensations and neuronal reflex behavior. The concept is that new antitussive drugs would have the benefit of targeting peripheral airway nociceptors without inhibiting the protective cough reflex.
Citace poskytuje Crossref.org
Literatura
- 000
- 00000naa a2200000 a 4500
- 001
- bmc21003476
- 003
- CZ-PrNML
- 005
- 20210228091127.0
- 007
- ta
- 008
- 210202s2020 xr f 000 0|eng||
- 009
- AR
- 024 7_
- $a 10.33549/physiolres.934395 $2 doi
- 035 __
- $a (PubMed)32228007
- 040 __
- $a ABA008 $b cze $d ABA008 $e AACR2
- 041 0_
- $a eng
- 044 __
- $a xr
- 100 1_
- $a Brozmanová, Mariana $7 xx0194153 $u Department of Pathophysiology, Jessenius Faculty of Medicine, Comenius University, Martin, Slovakia
- 245 14
- $a The Prospect for Potent Sodium Voltage-Gated Channel Blockers to Relieve an Excessive Cough / $c M. Brozmanova, N. Pavelkova
- 504 __
- $a Literatura
- 520 9_
- $a An excessive, irritable, productive or non-productive coughing associated with airway inflammation belongs to pathological cough. Increased activation of airway vagal nociceptors in pathological conditions results from dysregulation of the neural pathway that controls cough. A variety of mediators associated with airway inflammation overstimulate these vagal airway fibers including C-fibers leading to hypersensitivity and hyperreactivity. Because current antitussives have limited efficacy and unwanted side effects there is a continual demand for the development of a novel more effective antitussives for a new efficacious and safe cough treatment. Therefore, inhibiting the activity of these vagal C-fibers represents a rational approach to the development of effective antitussive drugs. This may be achieved by blocking inflammatory mediator receptors or by blocking the generator potential associated with the specific ion channels. Because voltage-gated sodium channels (NaVs) are absolutely required for action potentials initiation and conduction irrespective of the stimulus, NaVs become a promising neural target. There is evidence that NaV1.7, 1.8 and 1.9 subtypes are predominantly expressed in airway cough-triggering nerves. The advantage of blocking these NaVs is suppressing C-fiber irrespective to stimuli, but the disadvantage is that by suppressing the nerves is may also block beneficial sensations and neuronal reflex behavior. The concept is that new antitussive drugs would have the benefit of targeting peripheral airway nociceptors without inhibiting the protective cough reflex.
- 650 _2
- $a akční potenciály $x účinky léků $x fyziologie $7 D000200
- 650 _2
- $a zvířata $7 D000818
- 650 _2
- $a antitusika $x farmakologie $x terapeutické užití $7 D000996
- 650 _2
- $a kašel $x farmakoterapie $x patofyziologie $7 D003371
- 650 _2
- $a lidé $7 D006801
- 650 _2
- $a nociceptory $x účinky léků $x metabolismus $7 D009619
- 650 _2
- $a blokátory sodíkových kanálů řízených napětím $x farmakologie $x terapeutické užití $7 D061567
- 650 _2
- $a sodíkové kanálky řízené napětím $x fyziologie $7 D061566
- 655 _2
- $a časopisecké články $7 D016428
- 655 _2
- $a přehledy $7 D016454
- 700 1_
- $a Pavelková, Nikoleta $7 xx0257234 $u Department of Pathophysiology, Jessenius Faculty of Medicine, Comenius University, Martin, Slovakia
- 773 0_
- $w MED00003824 $t Physiological research $x 1802-9973 $g Roč. 69, Suppl 1 (2020), s. S7-S18
- 856 41
- $u https://pubmed.ncbi.nlm.nih.gov/32228007 $y Pubmed
- 910 __
- $a ABA008 $b A 4120 $c 266 $y p $z 0
- 990 __
- $a 20210202 $b ABA008
- 991 __
- $a 20210228091045 $b ABA008
- 999 __
- $a ok $b bmc $g 1624826 $s 1123778
- BAS __
- $a 3
- BAS __
- $a PreBMC
- BMC __
- $a 2020 $b 69 $c Suppl 1 $d S7-S18 $e 20200327 $i 1802-9973 $m Physiological research $n Physiol. Res. (Print) $x MED00003824
- LZP __
- $b NLK118 $a Pubmed-20210202