Cough is one of the most important defensive reflexes. However, extensive non- productive cough is a harmful mechanism leading to the damage of human airways. Cough is initiated by activation of vagal afferents in the airways. The site of their convergence is particularly the nucleus of the solitary tract (nTS). The second-order neurons terminate in the pons, medulla and spinal cord and there is also the cortical and subcortical control of coughing.Upper airway cough syndrome (UACS) - previously postnasal drip syndrome - is one of the most common causes of chronic cough together with asthma and gastroesophageal reflux. The main mechanisms leading to cough in patients with nasal and sinus diseases are postnasal drip, direct irritation of nasal mucosa, inflammation in the lower airways, upper airway inflammation and the cough reflex sensitization. The cough demonstrated by UACS patients is probably due to hypersensitivity of the upper airways sensory nerve or lower airways sensory nerve, or a combination of both. Further studies are needed to clarify this mechanism.
- MeSH
- chronická nemoc MeSH
- kapsaicin škodlivé účinky MeSH
- kašel chemicky indukované patofyziologie MeSH
- kationtové kanály TRPV agonisté fyziologie MeSH
- kationtový kanál TRPA1 agonisté fyziologie MeSH
- lidé MeSH
- nervové receptory účinky léků fyziologie MeSH
- nervus vagus účinky léků patofyziologie MeSH
- nosní sliznice účinky léků patofyziologie MeSH
- syndrom MeSH
- trachea účinky léků patofyziologie MeSH
- zvířata MeSH
- Check Tag
- lidé MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- přehledy MeSH
BACKGROUND: Chronic renal failure is frequently associated with a high risk of sudden cardiac death due to dysfunction of the autonomic nervous system. The pathogenic mechanisms underlying the parasympathetic cardiac dysautonomia are not fully elucidated yet. METHODS: Chronic renal failure was induced in rats by 5/6 nephrectomy. Blood pressure, resting heart rate and plasma levels of creatinine, urea and asymmetric dimethylarginine (ADMA) were measured. To characterize the parasympathetic innervation of the heart, chronotropic responses to atropine, metipranolol and to vagal stimulation in the absence or presence of ADMA were investigated in vivo. In vitro, chronotropic and inotropic effects of carbachol and ADMA and mRNA expression of muscarinic M2 receptors, high affinity choline transporter (CHT1), vesicular acetylcholine transporter (VAChT) and choline acetyltransferase (ChAT) were assessed in the isolated cardiac tissues. RESULTS: In 5/6 nephrectomy rats, the resting heart rate was significantly higher and the parasympathetic tone, measured as the effect of atropine after administration of metipranolol was significantly lower than in control animals. Plasma ADMA levels were significantly elevated in the uraemic rats and significantly inversely correlated with the effect of atropine on the heart rate. No differences were revealed in the plasma norepinephrine concentrations, negative chronotropic responses to stimulation of the vagus nerves, chronotropic and inotropic responses to carbachol and the relative expression of M2 receptors, CHT1, VAChT and ChAT. CONCLUSION: The data suggest that cardioacceleration in chronic renal failure is caused by a diminished cardiac parasympathetic tone in the presence of a functionally intact intrinsic cardiac cholinergic signalling system.
- MeSH
- atropin farmakologie MeSH
- beta blokátory farmakologie MeSH
- cholin-O-acetyltransferasa genetika metabolismus MeSH
- karbachol farmakologie MeSH
- kardiotonika farmakologie MeSH
- krysa rodu rattus MeSH
- ledviny chirurgie metabolismus účinky léků MeSH
- messenger RNA genetika metabolismus MeSH
- metipranolol farmakologie MeSH
- nefrektomie MeSH
- nervus vagus fyziologie účinky léků MeSH
- noradrenalin metabolismus MeSH
- parasympatický nervový systém fyziologie účinky léků MeSH
- parasympatolytika farmakologie MeSH
- polymerázová řetězová reakce s reverzní transkripcí MeSH
- potkani Wistar MeSH
- proteiny nervové tkáně genetika metabolismus MeSH
- proteiny přenášející neurotransmitery přes plazmatickou membránu genetika metabolismus MeSH
- srdce inervace MeSH
- srdeční frekvence fyziologie MeSH
- vezikulární transportní proteiny acetylcholinu genetika metabolismus MeSH
- western blotting MeSH
- zvířata MeSH
- Check Tag
- krysa rodu rattus MeSH
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- práce podpořená grantem MeSH
Vasoactive intestinal polypeptide (VIP) is implicated in the modulation of vagal effects on the heart rate. In this study, the impact of acute and chronic atropine administration on VIP levels in rat heart atria was investigated in relation to heart rate in the course of vagus nerves stimulation. Anaesthetised control and atropinised (10 mg/kg/day for 10 days) rats pretreated with metipranolol and phentolamine that were either given or not a single dose of atropine were subjected to bilateral vagus nerve stimulation (30 min: 0.7 mA, 20 Hz, 0.2 ms). VIP concentrations in the atria were determined after each stimulation protocol. In control rats with or without single atropine administration, the heart rate upon vagal stimulation was higher than in atropinised animals with or without single atropine dose, respectively. VIP concentrations in the control atria were significantly decreased after the stimulation; the decrease was comparable both in the absence and presence of a single dose of atropine. Compared to controls, VIP levels were significantly decreased after chronic atropine treatment and they were not further reduced by vagal stimulation and single atropine administration. Administration of VIP antagonist completely abolished the differences in the heart rate upon vagal stimulation between control and atropinised groups. In conclusion, the data indicate that chronic atropine administration affects VIP synthesis in rat heart atria and consequently it modifies the heart rate regulation.
- Klíčová slova
- Vasoactive intestinal polypeptide, Atropine, Heart atria, Vagus nerve stimulation, Rat,
- MeSH
- alfa blokátory farmakologie MeSH
- antagonisté hormonů farmakologie MeSH
- antagonisté muskarinových receptorů aplikace a dávkování MeSH
- atropin aplikace a dávkování MeSH
- beta blokátory farmakologie MeSH
- časové faktory MeSH
- elektrická stimulace MeSH
- fentolamin farmakologie MeSH
- financování organizované MeSH
- krysa rodu rattus MeSH
- metipranolol farmakologie MeSH
- nervus vagus metabolismus účinky léků MeSH
- potkani Wistar MeSH
- receptory muskarinové metabolismus účinky léků MeSH
- srdeční frekvence účinky léků MeSH
- srdeční síně inervace metabolismus MeSH
- vazoaktivní intestinální peptid antagonisté a inhibitory farmakologie metabolismus MeSH
- zvířata MeSH
- Check Tag
- krysa rodu rattus MeSH
- zvířata MeSH
- MeSH
- chemoreceptory účinky léků MeSH
- kontrakce myokardu genetika účinky záření MeSH
- lidé MeSH
- multiorgánové selhání mortalita patofyziologie terapie MeSH
- nemoci autonomního nervového systému farmakoterapie MeSH
- nervus vagus patofyziologie účinky léků MeSH
- presoreceptory účinky léků MeSH
- receptory cholinergní metabolismus účinky léků MeSH
- srdeční frekvence fyziologie účinky léků MeSH
- věkové faktory MeSH
- Check Tag
- lidé MeSH
- MeSH
- epilepsie terapie MeSH
- nervus vagus účinky léků MeSH
- refrakterní epilepsie terapie MeSH
- Publikační typ
- kongresy MeSH
- MeSH
- celková anestezie škodlivé účinky MeSH
- dospělí MeSH
- laryngoskopie škodlivé účinky MeSH
- lidé MeSH
- nervus vagus patofyziologie účinky léků MeSH
- sinus caroticus patofyziologie účinky léků MeSH
- srdeční zástava etiologie patologie MeSH
- vazomotorický systém patofyziologie účinky léků MeSH
- Check Tag
- dospělí MeSH
- lidé MeSH
- mužské pohlaví MeSH
- Publikační typ
- kazuistiky MeSH
