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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Prostanoid-induced blood-aqueous barrier breakdown in rabbits involves the EP2 receptor subtype.

Previous studies on prostanoid-induced blood-aqueous barrier disruption have been predominantly restricted to studies on natural prostanoids and the highly selective DP-receptor agonist BW245C, which was inactive. The pharmacology of prostanoid-induced blood-aqueous barrier breakdown in rabbits has been extended in these studies by determining the activity of additional prostanoid receptor agonists which are relatively selective according to the current classification for prostanoid receptors. Prostanoid effects were evaluated by measuring plasma albumin leakage into the aqueous humor as an indicator of blood-aqueous barrier breakdown. EP1 and EP3 receptor subtype agonists were ineffective in altering the blood-aqueous barrier, but the relatively selective EP2 agonist 11-deoxy prostaglandin E1 had a dose-dependent disruptive effect on the blood-aqueous barrier. In contrast, FP, IP and TP receptor agonists were ineffective in disrupting the blood-aqueous barrier. Taken together, these data imply that the EP2 receptor subtype, as a singular entity, may account for the rapid disruption of the rabbit blood-aqueous barrier that typically occurs in response to prostanoids.[1]


  1. Prostanoid-induced blood-aqueous barrier breakdown in rabbits involves the EP2 receptor subtype. Protzman, C.E., Woodward, D.F. Invest. Ophthalmol. Vis. Sci. (1990) [Pubmed]
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