1. The effects of intracameral injections of prostaglandins E1, E2, Fia, F2a, and A1 were studied on.the intraocular pressure (IOP) of rabbits anaesthetized with urethane.2. With the exception of prostaglandin F,a, all the prostaglandins studied were found to be capable of producing a large, sustained rise in IOP, accompanied in many cases by miosis. 3. A marked decrease in response to repeated injections was found with all the prostaglandins studied; this effect was more pronounced following a large initial response to the prostaglandin. 4. The descending order of potency in their ability to raise IOP was as follows: prostaglandin Ei-E2>F2a>Al>Fia.5. Intracameral injections of prostaglandins E1 and E2 resulted in an increase in the protein content of the aqueous humour, which was related to the magnitude of the sustained increase in IOP. 6. Stabilization of the blood-aqueous barrier with polyphloretin phosgphate markedly reduced both the IOP response and the effect of prostaglandin E2 on the protein content of the aqueous humour. 7. It is concluded that the production of local vasodilatation and increased permeability of the blood-aqueous barrier play an important part in the effect of prostaglandins on the IOP. The involvement of prostaglandins in the response of the rabbit eye to irritation is discussed.Injections of prostaglandins into rabbit eyes have been shown by Waitzman & King (1967) to produce a sustained rise in intraocular pressure (IOP). This effect on the IOP was thought to result from an action of prostaglandins on the metabolic processes involved in aqueous humour production, rather than from vascular or permeaibility changes (Waitzman, 1968), although it was well known that many prostaglandins are powerful vasodilators. Moreover, it had been shown earlier that the response of the rabbit eye to irritation is associated with the release into the aqueous humour of irin, an ether-soluble spasmogen with vasodilator activity consisting of unsaturated hydroxy fatty acid(s)

Summary. Prostaglandins (El, E 2 and F2~ ) stimulated the chloride transport of the frog corneal epithelium with maximal effects at 10 -5 M in the aqueous side. This stimulation does not occur in Cl-free solutions and the net 36C1 flux increased proportionally to the short-circuit current. Polyphloretin phosphate (PPP) and diphloretin phosphate (DPP) inhibited the response if added within 3 rain before PGE 1. The maximal response to epinephrine 10-SM and dibutyryl cyclic AMP 10-3M was not changed by further addition of prostaglandins, but these drugs produced their full effect when administered at the peak of the response of prostaglandins. The maximal response to theophylline 10 -5 M was increased by PGE 1. PPP and DPP did not modify the response to epinephrine. Prostaglandin stimulation of the chloride transport was accompanied by increased light transmission through partially opaque corneas. The known release of prostaglandins in the aqueous humor can be associated to a direct action on the corneal epithelium manifested in the activation described herein.The transparency of the cornea is dependent on the state of hydration of the stroma. The two principal cell layers of this tissue, the epithelium in front, and the endothelium inside, contribute by their permeability properties and, by the presence of ionic pumps, to the control of the state of hydration of the stroma (Maurice, 1969;.The epithelium of the frog cornea transports chloride ions out into the tear side (Zadunaisky, 1966), and this mechanism has been shown to be

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