Centrally injected CDP-choline increases plasma vasopressin levels by central cholinergic activation


Cavun S., Savci V., Ulus I.

Fundamental and Clinical Pharmacology, cilt.18, sa.1, ss.71-77, 2004 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 18 Sayı: 1
  • Basım Tarihi: 2004
  • Doi Numarası: 10.1046/j.0767-3981.2003.00213.x
  • Dergi Adı: Fundamental and Clinical Pharmacology
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.71-77
  • Anahtar Kelimeler: CDP-choline, choline, cytidine, nicotinic receptor, precursor, vasopressin, RAT SUPRAOPTIC NUCLEUS, CONSCIOUS RATS, ACETYLCHOLINE-RECEPTORS, RELEASE, NEURONS, HYPOTHALAMUS, INVOLVEMENT, HIPPOCAMPAL, HEMORRHAGE, CITICOLINE
  • Bursa Uludağ Üniversitesi Adresli: Evet

Özet

In the present study, both the effects of intracerebroventricular (i.c.v.) injection of cytidine-5′-diphosphate choline (CDP-choline) on plasma vasopressin levels and the choline involvement of these effects were investigated. I.c.v. administration of CDP-choline (0.5, 1.0 and 2.0 μmol) increased plasma vasopressin levels dose- and time-dependently. I.c.v. injection of equimolar dose of choline (1 μmol) produced similar vasopressin response. However equimolar dose of cytidine (1 μmol; i.c.v.), the other hydrolysis product of CDP-choline, did not affect plasma vasopressin levels. Pretreatment of rats with hemicholinium-3, neuronal high affinity choline uptake inhibitor (20 μg; i.c.v.) blocked the vasopressin response to i.c.v. CDP-choline (1 μmol). Pretreatment of rats with mecamylamine (50 μg; i.c.v.), a nonselective nicotinic receptor antagonist, abolished the increase in plasma vasopressin induced by CDP-choline while atropine (10 μg; i.c.v.), nonselective muscarinic receptor antagonist, failed to change the response. In conclusion, intracerebroventricularly injected CDP-choline can increase plasma vasopressin levels by activating central nicotinic cholinergic receptors through the activation of presynaptic cholinergic mechanisms.