INTERACTION OF ADRENERGIC AGENTS WITH ALPHA-MELANOCYTE-STIMULATING HORMONE AND IR IRRADIATION OF IRIS IN RABBIT EYE

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  • 1 January 1977
    • journal article
    • research article
    • Vol. 16  (3) , 209-217
Abstract
Breakdown of the blood aqueous barrier in the rabbit eye induces a protein leakage into the aqueous humor, seen as a flare in the anterior chamber. A barrier damage was induced by topical prostaglandin E2(PGE2), IR irradiation of the iris, or .alpha.-melanocyte-stimulating hormone (.alpha.-MSH) given s.c. The aqueous flare was measured quantitatively by a photoelectric instrument. Interference of adrenergic antagonists and agonists on breakdown of the barrier was tested. The .alpha.-adrenergic antagonist phentolamine and the .beta.-adrenergic antagonist propranolol, given i.v., had no effect on exogenously administered PGE2, but both antagonists reduced the flare response to IR irradiation which is supposed to exert its effect via endogenous prostaglandin release. The .alpha.-MSH response was unaffected by phentolamine, whereas propranolol abolished the flare response to .alpha.-MSH totally. The PGE2 response was unaffected both by the .alpha.-adrenergic agonist noradrenaline [norepinephrine] and the .beta.-adrenergic agonist terbutalin sulfate, administered topically. Noradrenaline inhibited the flare response to IR irradiation and facilitated the flare response to .alpha.-MSH. Terbutalin sulfate worked synergistically with both IR irradiation and .alpha.-MSH. .alpha.-MSH probably exerts its effect on the barrier via enhanced .beta.-adrenergic activity, whereas effects caused by IR irradiation seem conditioned by intact .alpha.- and .beta.-adrenergic receptor sites.

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