HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 290/3/H1182    most recent 00280.2005v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (2) Citing Articles via Google Scholar Google Scholar Articles by Stähli, B. E. Articles by Tanner, F. C. Search for Related Content PubMed PubMed Citation Articles by Stähli, B. E. Articles by Tanner, F. C.

Absence of histamine-induced nitric oxide release in the human radial artery: implications for vasospasm of coronary artery bypass vessels

¹Cardiovascular Research, Physiology Institute and Center for Integrative Human Physiology, University of Zürich, and Department of Cardiology, Cardiovascular Center, University Hospital, Zürich; ²Cardiovascular Research, Department of Clinical Research, University of Bern and Clinic for Cardiovascular Surgery, University Hospital, Bern; ³Clinic for Cardiovascular Surgery, Cardiovascular Center, University Hospital, Zürich; and ⁴Dermatology, University Hospital, Zürich, Switzerland

Submitted 22 March 2005 ; accepted in final form 12 October 2005

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-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.

endothelium-dependent relaxation; heterogeneity; receptor

This article has been cited by other articles:

				Y. Zhang, T. Tazzeo, V. Chu, and L. J. Janssen Membrane potassium currents in human radial artery and their regulation by nitric oxide donor Cardiovasc Res, July 15, 2006; 71(2): 383 - 392. [Abstract] [Full Text] [PDF]