The effect of centrally injected CDP-choline on respiratory system; involvement of phospholipase to thromboxane signaling pathway
Autor: | Trevor F.C. Batten, Burcin Altinbas, Bora B. Topuz, Sikha Saha, Murat Yalcin, Mustafa Sertac Yilmaz, Vahide Savci |
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Rok vydání: | 2014 |
Předmět: |
Male
Pulmonary and Respiratory Medicine medicine.medical_specialty Cytidine Diphosphate Choline Time Factors Physiology Thromboxane Respiratory System Agents Phospholipase Rats Sprague-Dawley Respiratory Rate Internal medicine Hyperventilation Mecamylamine Tidal Volume medicine Animals Injections Intraventricular Phospholipase A Dose-Response Relationship Drug Phospholipase C Chemistry General Neuroscience Thromboxanes Rats carbohydrates (lipids) Endocrinology Nicotinic agonist Phospholipases Cholinergic lipids (amino acids peptides and proteins) medicine.symptom Signal Transduction medicine.drug |
Zdroj: | Respiratory Physiology & Neurobiology. 195:50-58 |
ISSN: | 1569-9048 |
DOI: | 10.1016/j.resp.2014.02.005 |
Popis: | CDP-choline is an endogenous metabolite in phosphatidylcholine biosynthesis. Exogenous administration of CDP-choline has been shown to affect brain metabolism and to exhibit cardiovascular, neuroendocrine neuroprotective actions. On the other hand, little is known regarding its respiratory actions and/or central mechanism of its respiratory effect. Therefore the current study was designed to investigate the possible effects of centrally injected CDP-choline on respiratory system and the mediation of the central cholinergic receptors and phospholipase to thromboxane signaling pathway on CDP-choline-induced respiratory effects in anaesthetized rats. Intracerebroventricularly (i.c.v.) administration of CDP-choline induced dose- and time-dependent increased respiratory rates, tidal volume and minute ventilation of male anaesthetized Spraque Dawley rats. I.c.v. pretreatment with atropine failed to alter the hyperventilation responses to CDP-choline whereas mecamylamine, cholinergic nicotinic receptor antagonist, mepacrine, phospholipase A 2 inhibitor, and neomycin phospholipase C inhibitor, blocked completely the hyperventilation induced by CDP-choline. In addition, central pretreatment with furegrelate, thromboxane A 2 synthesis inhibitor, also partially blocked CDP-choline-evoked hyperventilation effects. These data show that centrally administered CDP-choline induces hyperventilation which is mediated by activation of central nicotinic receptors and phospholipase to thromboxane signaling pathway. |
Databáze: | OpenAIRE |
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