Possible role of histamine (H1- and H2-) receptors in the regulation of meningeal blood flow
Version of Record online: 2 FEB 2009
2002 British Pharmacological Society
British Journal of Pharmacology
Volume 137, Issue 6, pages 874–880, November 2002
How to Cite
Dux, M., Schwenger, N. and Messlinger, K. (2002), Possible role of histamine (H1- and H2-) receptors in the regulation of meningeal blood flow. British Journal of Pharmacology, 137: 874–880. doi: 10.1038/sj.bjp.0704946
- Issue online: 2 FEB 2009
- Version of Record online: 2 FEB 2009
- (Received August 13, 2002, Accepted August 28, 2002)
- Dura mater encephali;
- arterial blood flow;
Vasodilatation in the dura mater has been suggested to play an important role in the pathophysiology of vascular headaches. Histamine may contribute to these vascular changes. The aim of the present study was to examine the role of different histamine receptors in histamine-induced meningeal hyperperfusion using laser Doppler flowmetry.
The blood flow in the medial meningeal artery was monitored in the exposed parietal dura mater encephali of barbiturate anaesthetized rats. Local application of histamine (10−5 and 10−4M) onto the dura caused increases in flow to 114.2±9.6 and 135.1±19.1%, respectively, of the basal flow.
Flow increases induced by topical application of histamine (10−4M) were reduced by local pretreatment with the H2-receptor antagonist cimetidine (0.4 and 4 mM) to 63.4±17 and 37.8±18.8%, respectively. Systemic pre-administration of cimetidine (5 mg kg−1 i.v.) did not change histamine-induced flow increases.
Local pretreatment with the H1-receptor antagonist cetirizine (2 μM) further increased the flow evoked by topical histamine administration (10−4M) to 123.5±14.7% of the histamine control.
Increases in blood flow induced by i.v. administration of histamine (10 μg kg−1) were reduced by i.v. pre-injection of cetirizine (50 μg kg−1) to 31.9±9% but not by i.v. cimetidine (5 mg kg−1).
We conclude that histamine-induced relaxation of dural arterial vessels is mediated by H2-receptors, most likely located on vascular smooth muscle cells, and by endothelial H1-receptors. In addition, H1-receptors on smooth muscle cells may mediate vasoconstriction.
British Journal of Pharmacology (2002) 137, 874–880. doi:10.1038/sj.bjp.0704946