Does prostacyclin mediate alpha-adrenergic induced hypotension?

We have extended our previous observations on the effect of tranylcypromine (TCP) on intraocular pressure (IOP), following topical administration of catecholamines is normal and chemically denervated rabbit eyes. In normal eyes, TCP inhibits the hypotensive phase after topical norepinephrine (nE); less after epinephrine (E); and not at all after isoproterenol. In denervated eyes, the inhibitory effect of TCP on the hypotensive phase of nE and E is enhanced. Phenoxybenzamine (PBA), but not timolol maleate or indomethacin, blocks the effect of TCP on alpha-adrenergic induced hypotension. Prostacyclin-like activity was estimated by bioassay using ADP induced rat platelet aggregation. This activity is significantly reduced in the primary aqueous and in the iris after TCP but it is significantly increased in pooled data of aqueous samples after topical nE. We conclude that the inhibitory effect of TCP on the hypotensive phase after topical E and nE is the result of inhibition of prostacyclin synthesis and not of MAO inhibition nor blockade of alpha-receptors. It is possible that the normal production of prostacyclin by the iris and ciliary body maintains (lower) basal levels of IOP.