Mechanisms of histamine-induced relaxation in external and internal ophthalmic arteries.

PURPOSE

Mechanisms that underlie the relaxant response to histamine were examined in dog external (a branch of external carotid artery) and internal (a branch of internal carotid artery) ophthalmic arteries (EOA and IOA).

METHODS

Changes in isometric tensions were recorded in helical strips of the arteries with and without the endothelium.

RESULTS

Histamine predominantly produced relaxations in EOA and IOA, partially contracted with prostaglandin (PG) F2 alpha. The relaxation of IOA almost was abolished by treatment with cimetidine (10(-5) mol/l), whereas the response of EOA was partially attenuated by treatment with cimetidine or chlorpheniramine (10(-6) mol/l) and was abolished with their combined treatment. Endothelium denudation depressed the relaxation in EOA but did not affect the response of IOA. The response to histamine of EOA was inhibited by treatment with indomethacin (10(-6) mol/l) or tranylcypromine (10(-4) mol/l), a PGI2 synthesis inhibitor, only when the endothelium was present, but additional treatment with chlorpheniramine did not further inhibit relaxation. On the other hand, IOA's response to histamine was not inhibited by indomethacin, despite the presence of endothelium.

CONCLUSIONS

The histamine-induced relaxation in EOA may be associated with the release of vasodilator PGI2 through the activation of H1 receptors in the endothelium and with the direct action on H2 receptors in smooth muscle, whereas the relaxation in IOA is mediated exclusively by H2 receptors in smooth muscle.