Pharmacological analysis of vasoconstriction of isolated canine ophthalmic and ciliary arteries to alpha-adrenoceptor agonists.

Effects of five alpha-adrenoceptor agonists were investigated on the canine internal, external ophthalmic and ciliary arteries by the use of several kinds of antagonists. These arteries were isolated with the optic nerve and perfused with Tyrode solution under a constant flow rate at 37 degrees C. Control perfusion pressure was within 40-80 mmHg. Each drug solution except sodium nitroprusside (SNP) was administered by a microinjector into the endothelial side of the artery through a cannulated tubing, and SNP was administered by being dissolved into the perfusion solution. The response was obtained as changes in perfusion pressure. Results were as follows: (1) epinephrine (EPI), norepinephrine (NE), phenylephrine (PHE), and KCl induced a marked vasoconstriction in these arteries, although xylazine (XYL) and clonidine (CLO) did not produce any significant change; (2) bunazosin, a potent alpha-1 adrenoceptor blocker, antagonized the effects of NE and PHE in a dose-related manner, and did not affect the responses to KCl; (3) diltiazem reduced the KCl-induced vasoconstriction in a dose-related manner, and it did not significantly influence the vascular responses to NE; (4) SNP reduced the NE-induced vasoconstriction but the KCl-induced vasoconstriction was only suppressed by a large dose of SNP. From these results, it is suggested that; (1) these arteries contain alpha-1 but not alpha-2 adrenoceptors; (2) NE-induced vasoconstriction is independent of the Ca2+ inward current but probably involves intracellular Ca2+ ion movement; (3) SNP may influence intracellular Ca2+ movement in these arteries.