ABSTRACTPurpose.Mechanisms underlying the relaxant response to histamine were compared in isolated dog retinal arteries (branch of internal and external carotid arteries), middle cerebral arteries (branch of internal carotid artery) and superficial temporal arteries (branch of external carotid artery).Methods.Changes in the isometric tension of helical strips of the arteries with and without the endothelium were recorded.Results.Histamine produced concentration-related biphasic (phasic and sustained) relaxations in retinal arterial strips contracted partially with prostaglandin (PG)F2α. Relaxations induced by histamine were not dependent on the endothelium. Treatment with cimetidine attenuated the sustained relaxation, whereas chlorpheniramine or indomethacin depressed the phasic relaxation. In addition, the phasic relaxant response to histamine was attenuated by tranylcypromine, a PGI2synthesis inhibitor. In contrast, the amine-induced relaxant responses in dog middle cerebral arterial branch and temporal arteries were markedly suppressed by cimetidine alone.Conclusions.In dog retinal arteries, the phasic relaxation caused by histamine is mediated by PGI2in association with activation of the H1receptor subtype in subendothelial tissues, possibly smooth muscle, and the sustained relaxation is evoked by direct stimulation of the H2receptor subtype in smooth muscle. The histamine-induced relaxation in temporal and distal middle cerebral arteries is associated solely with a stimulation of H2receptors in smooth muscle
展开▼