title: Absence of histamine-induced nitric oxide release in the human radial artery: implications for vasospasm of coronary artery bypass vessels.
abstract: Radial artery (RA) bypass grafts can develop severe vasospasm. As histamine is known to induce vasospasm, its effect on RA was assessed compared with the classic bypass vessels internal mammary artery (MA) and saphenous vein (SV). The vessels were examined in organ chambers for isometric tension recording. Histamine induced contractions on baseline; the sensitivity was higher in RA and SV than MA. After precontraction with norepinephrine, histamine did not evoke relaxations of RA but induced relaxations of MA and less of SV at lower concentrations; it induced contractions at higher concentrations, reaching similar levels in all three vessels. Indomethacin did not affect the response of MA and RA but potentiated relaxations and reduced contractions of SV. Endothelium removal, N(omega)-nitro-L-arginine methyl ester (L-NAME), or the H2-receptor blocker cimetidine did not affect the response of RA, but inhibited relaxations and enhanced contractions in MA and inhibited relaxations in SV; in the latter, only L-NAME enhanced contractions. Real-time PCR detected much lower expression of endothelial H2-receptor in RA than MA or SV. Western blots revealed similar endothelial nitric oxide (NO) synthase expression in all three vessels. Relaxations to acetylcholine were identical in RA and MA. Thus histamine releases NO by activating the endothelial H2-receptor, the expression of which is much lower in RA than MA or SV. H2-receptor activation also releases prostaglandins in SV, partially antagonizing NO. The lack of histamine-induced NO production represents a possible mechanism of RA vasospasm.
authors.affiliation: Cardiovascular Research, Physiology Institute and Center for Integrative Human Physiology, University of Zürich, Winterthurerstrasse 190, 8057 Zürich, Switzerland.
authors.forename: Barbara E
authors.initials: BE
authors.lastname: Stähli
authors.forename: Helen
authors.initials: H
authors.lastname: Greutert
authors.forename: Shaoping
authors.initials: S
authors.lastname: Mei
authors.forename: Philipp
authors.initials: P
authors.lastname: Graf
authors.forename: Karin
authors.initials: K
authors.lastname: Frischknecht
authors.forename: Mario
authors.initials: M
authors.lastname: Stalder
authors.forename: Lars
authors.initials: L
authors.lastname: Englberger
authors.forename: Andreas
authors.initials: A
authors.lastname: Künzli
authors.forename: Leo
authors.initials: L
authors.lastname: Schärer
authors.forename: Thomas F
authors.initials: TF
authors.lastname: Lüscher
authors.forename: Thierry P
authors.initials: TP
authors.lastname: Carrel
authors.forename: Felix C
authors.initials: FC
authors.lastname: Tanner
mesh_terms: D001026:Coronary Artery Bypass / Q000379:methods; D003329:Coronary Vasospasm / Q000503:physiopathology; D003331:Coronary Vessels / Q000503:physiopathology / Q000637:transplantation; D004305:Dose-Response Relationship, Drug; D004730:Endothelium, Vascular / Q000187:drug effects / Q000502:physiology*; D006632:Histamine / Q000008:administration & dosage*; D006801:Humans; D066298:In Vitro Techniques; D008323:Mammary Arteries / Q000187:drug effects / Q000502:physiology*; D009569:Nitric Oxide / Q000096:biosynthesis*; D017534:Radial Artery / Q000187:drug effects / Q000502:physiology*; D012501:Saphenous Vein / Q000187:drug effects / Q000502:physiology*; D014664:Vasodilation / Q000187:drug effects / Q000502:physiology*
chemical_list: D009569:Nitric Oxide; D006632:Histamine