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Ocular hypertensive response to beta-adrenoceptor agonists.

D E Potter, H T Nicholson, J M Rowland

    Current Eye Research
    |January 1, 1982
    PubMed
    Summary

    Topical beta-agonists can cause ocular hypertension with repeated use, unlike single doses. This effect, particularly with the levorotatory form, may involve increased aqueous humor production, as shown in rabbit models.

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    Area of Science:

    • Ophthalmology
    • Pharmacology
    • Ocular Physiology

    Background:

    • Beta-adrenoceptor agonists are commonly used to lower intraocular pressure (IOP).
    • Acute administration typically results in a decrease in IOP.
    • The effects of chronic or repeated administration are less understood.

    Purpose of the Study:

    • To investigate the effects of repeated topical administration of beta-adrenoceptor agonists on IOP in rabbits.
    • To compare the hypertensive potential of different beta-agonist enantiomers.
    • To explore the potential mechanism behind the observed IOP changes.

    Main Methods:

    • Unilateral topical application of 2% beta-agonist solutions (l-epinephrine, reproterol, l-isoproterenol, d-isoproterenol) in normal and surgically altered rabbits.
    • Daily administration for consecutive days.
    • Assessment of IOP changes.
    • Inhibition studies using timolol.

    Main Results:

    • Repeated topical application of l-epinephrine, reproterol, and l-isoproterenol caused significant ocular hypertension.
    • d-isoproterenol showed only hypotensive responses even with repeated administration.
    • The hypertensive effect was enantiomer-specific, with the levorotatory form being more potent.
    • Timolol inhibited the hypertensive effects of epinephrine and reproterol.

    Conclusions:

    • Chronic topical beta-agonist use can lead to ocular hypertension, contrary to acute effects.
    • The mechanism may involve increased aqueous humor production, as suggested by timolol's inhibitory effect.
    • Enantioselectivity plays a role in the hypertensive response to beta-agonists.

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