Influences of cyclic nucleotides on outflow facility in the vervet monkey

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Analogues of adenosine 3′,5′-monophosphate (cyclic AMP), such as 8-methylthio cyclic AMP or dibutyryl cyclic AMP, administered into the anterior chamber of the vervet monkey eye, in vivo, cause a two-fold increase in outflow facility which lasts approximately 1 hr. Isoproterenol, given intracamerally, increases outflow facility, as demonstrated previously by other investigators. Intracameral pretreatment with isoproterenol prevents a further increase in outflow facility following a cyclic AMP analogue, perfused through the anterior chamber. Topical epinephrine also increases outflow facility as shown previously by other investigators. Topical pretreatment with epinephrine prevents a further increase in outflow facility following a cyclic AMP analogue, given intracamerally. These findings indicate that the primary action of catecholamines on outflow facility in the primate is mediated by cyclic AMP. To determine if the cholinergic action on outflow facility is mediated by an intracellular messenger, a potent analogue of guanosine 3′,5′-monophosphate was tested and found to be ineffective. Perfusion of 8-methylthio cyclic AMP through the anterior chamber of the enucleated vervet monkey eye causes a decrease in outflow facility. These results, in vitro, are opposite to those observed in vivo and may be due to cyclic AMP-induced relaxation of the ciliary muscle.