title: Carbon monoxide-prostaglandin E2 interaction in the hypothalamic circulation.
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 E2 (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.
authors.affiliation: Institute of Human Physiology and Clinical Experimental Research, Molecular Biology and Pathobiochemistry, Semmelweis University, Budapest, Hungary.
authors.forename: Béla
authors.initials: B
authors.lastname: Horváth
authors.forename: László
authors.initials: L
authors.lastname: Hortobágyi
authors.forename: Gábor
authors.initials: G
authors.lastname: Lenzsér
authors.forename: Horst
authors.initials: H
authors.lastname: Schweer
authors.forename: András
authors.initials: A
authors.lastname: Hrabák
authors.forename: Péter
authors.initials: P
authors.lastname: Sándor
authors.forename: Zoltán
authors.initials: Z
authors.lastname: Benyó
mesh_terms: D015121:6-Ketoprostaglandin F1 alpha / Q000134:cerebrospinal fluid / Q000378:metabolism; D000818:Animals; D001784:Blood Gas Analysis / Q000379:methods; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D002248:Carbon Monoxide / Q000378:metabolism*; D016861:Cyclooxygenase Inhibitors / Q000008:administration & dosage / Q000494:pharmacology; D003905:Deuteroporphyrins / Q000008:administration & dosage / Q000494:pharmacology; D004008:Diclofenac / Q000008:administration & dosage / Q000494:pharmacology; D015237:Dinoprost / Q000134:cerebrospinal fluid / Q000378:metabolism; D015232:Dinoprostone / Q000134:cerebrospinal fluid / Q000378:metabolism*; D004791:Enzyme Inhibitors / Q000008:administration & dosage / Q000494:pharmacology; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology; D006419:Heme Oxygenase (Decyclizing) / Q000037:antagonists & inhibitors / Q000378:metabolism*; D007031:Hypothalamus / Q000098:blood supply* / Q000187:drug effects / Q000378:metabolism; D007274:Injections, Intraperitoneal; D007275:Injections, Intravenous; D008297:Male; D019331:NG-Nitroarginine Methyl Ester / Q000008:administration & dosage / Q000494:pharmacology; D015230:Prostaglandin D2 / Q000134:cerebrospinal fluid / Q000378:metabolism; D011451:Prostaglandin-Endoperoxide Synthases / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar
chemical_list: D016861:Cyclooxygenase Inhibitors; D003905:Deuteroporphyrins; D004791:Enzyme Inhibitors; C060750:zinc deuteroporphyrin IX 2,4-bis(glycol); D004008:Diclofenac; D015121:6-Ketoprostaglandin F1 alpha; D002248:Carbon Monoxide; D015237:Dinoprost; D006419:Heme Oxygenase (Decyclizing); D011451:Prostaglandin-Endoperoxide Synthases; D015232:Dinoprostone; D015230:Prostaglandin D2; D019331:NG-Nitroarginine Methyl Ester