MOXONIDINE-INDUCED INHIBITION OF NOREPINEPHRINE RELEASE IN MONKEY ANDRABBIT CILIARY BODIES - ROLE OF CGMP

This study was designed to determine whether in isolated rabbit iris-c iliary bodies and monkey ciliary bodies, cGMP plays a role in the acti on of moxonidine, an alpha 2- and imidazoline (I-1) receptor agonist. In field-stimulated rabbit iris-ciliary bodies, dose-related inhibitio n of norepinephrine release was induced by 8-Br-cGMP, moxonidine or so dium nitroprusside; 8-Br-cGMP in combination with moxonidine did not e nhance inhibition of norepinephrine release. Sodium nitroprusside at i ntermediate and high concentrations stimulated cGMP production in rabb it iris-ciliary bodies, whereas moxonidine stimulated cGMP production modestly only at a high concentration. When iris-ciliary bodies were p retreated with a low concentration of moxonidine, sodium nitroprusside -stimulated cGMP production was enhanced from 1.6 to 2.2 pmol/mg prote in. In field-stimulated monkey ciliary bodies, both sodium nitroprussi de and moxonidine inhibited norepinephrine release. Pretreatment of el ectrically stimulated monkey ciliary bodies with sodium nitroprusside enhanced the suppressive effect of moxonidine on norepinephrine releas e. In monkey ciliary bodies, moxonidine raised cGMP production more th an sodium nitroprusside did, but there was no synergism in cGMP produc tion by combined treatment with moxonidine and sodium nitroprusside. T hese results suggest that cGMP could play a role in the ocular action( s) of moxonidine in ciliary bodies; however, involvement of cGMP in th e action of moxonidine in monkey ciliary bodies seems to be more prono unced than in rabbit iris-ciliary bodies.