Carbon monoxide-prostaglandin E2 interaction in the hypothalamic circulation

Béla Horváth, László Hortobágyi, Gábor Lenzsér, Horst Schweer, András Hrabák, Péter Sándor, Zoltán Benyó

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5 Citations (Scopus)

Abstract

The heme oxygenase (HO)-carbon monoxide pathway was earlier shown to increase hypothalamic blood flow after inhibition of nitric oxide synthesis in rats. We hypothesized that this effect is mediated by prostaglandin E 2 (PGE2). Inhibition of constitutive HO activity decreased cerebral PGE2 production and simultaneously increased hypothalamic nitric oxide synthase (NOS) activity without changing hypothalamic blood flow. Furthermore, HO blockade induced cyclooxygenase-dependent decrease and NOS-mediated increase of the hypothalamic blood flow after inhibition of NOS and cyclooxygenase, respectively. Therefore, constitutive carbon monoxide release seems to have two indirect effects on the hypothalamic circulation: vasodilation mediated by PGE2 and vasoconstriction as a result of NOS inhibition.

Original languageEnglish
Pages (from-to)1601-1604
Number of pages4
JournalNeuroreport
Volume19
Issue number16
DOIs
Publication statusPublished - Oct 29 2008

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Keywords

  • Carbon monoxide
  • Cerebral circulation
  • Cyclooxygenase
  • Heme oxygenase
  • Hypothalamus
  • Nitric oxide synthase
  • Prostaglandin E

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Horváth, B., Hortobágyi, L., Lenzsér, G., Schweer, H., Hrabák, A., Sándor, P., & Benyó, Z. (2008). Carbon monoxide-prostaglandin E2 interaction in the hypothalamic circulation. Neuroreport, 19(16), 1601-1604. https://doi.org/10.1097/WNR.0b013e3283129790