The effect of centrally injected CDP-choline on respiratory system; involvement of phospholipase to thromboxane signaling pathway

Topuz B. B., Altinbas B., Yilmaz M. S., Saha S., Batten T. F., SAVCI V., ...Daha Fazla

Respiratory Physiology and Neurobiology, cilt.195, sa.1, ss.50-58, 2014 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 195 Sayı: 1
  • Basım Tarihi: 2014
  • Doi Numarası: 10.1016/j.resp.2014.02.005
  • Dergi Adı: Respiratory Physiology and Neurobiology
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.50-58
  • Anahtar Kelimeler: CDP-choline, Intracerebroventricular, Respiratory frequency, Tidal volume, Minute ventilation, Central prostaglandinergic system, Central cholinergic receptors, INCREASES PLASMA VASOPRESSIN, ARACHIDONIC-ACID, BRAIN, RAT, PRESSOR, ACTIVATION, A(2), HYPOTENSION, CYTIDINE, RECEPTOR
  • Bursa Uludağ Üniversitesi Adresli: Evet

Özet

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. İ.c.v. pretreatment with atropine failed to alter the hyperventilation responses to CDP-choline whereas mecamylamine, cholinergic nicotinic receptor antagonist, mepacrine, phospholipase A2 inhibitor, and neomycin phospholipase C inhibitor, blocked completely the hyperventilation induced by CDP-choline. In addition, central pretreatment with furegrelate, thromboxane A2 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. © 2014 Elsevier B.V.