Histamine actions in dog retinal central arteries as compared to those in middle cerebral and temporal arteries.

PURPOSE

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)F2 alpha. 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 PGI2 synthesis 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 PGI2 in association with activation of the H1 receptor subtype in subendothelial tissues, possibly smooth muscle, and the sustained relaxation is evoked by direct stimulation of the H2 receptor subtype in smooth muscle. The histamine-induced relaxation in temporal and distal middle cerebral arteries is associated solely with a stimulation of H2 receptors in smooth muscle.