title: In vivo cAMP level in rabbit iris-ciliary body after topical epinephrine treatment.
abstract: OBJECTIVE
  The present study estimates the in vivo cyclic AMP (cAMP) level in the rabbit iris-ciliary body after topical treatment with epinephrine.
  
  
  METHODS
  Epinephrine 1% was applied unilaterally to pigmented rabbits. At selected time points between 10 min and 6 hr, a 2.5-mm diameter iris-ciliary body, in the treated eye, was irradiated with 2 J diode laser (2 W for 1 sec). Instant heat generated by the irradiation deactivated the cellular enzymes used in the synthesis and degradation of cAMP. Rabbits were sacrificed immediately, and samples of the iris-ciliary body were isolated from the irradiated area, the non-irradiated area, and from the contralateral, untreated eye. Levels of cAMP in these samples and in the aqueous humor were determined by radioimmunoassay. Further experiments were performed in rabbits pretreated with an alpha 2-adrenergic antagonist, yohimbine, and a beta-adrenergic antagonist, timolol, 30 min before the epinephrine treatment. Unilateral laser photocoagulation of the iris-ciliary body was performed at 10 min and 1 hr after the epinephrine treatment.
  
  
  RESULTS
  The cAMP level in the photocoagulated iris-ciliary body did not change in parallel to the change in the aqueous humor. An increase of aqueous humor cAMP was observed for 6 hr. However, a reduction of cAMP level in the photocoagulated iris-ciliary body was observed at 1 hr after the epinephrine treatment. In yohimbine-pretreated rabbits, the reduction of cAMP level in the photocoagulated iris-ciliary body was absent. Pretreatment with timolol had no effect.
  
  
  CONCLUSIONS
  These observations suggest that, at 1 hr after the epinephrine treatment, the cellular signal via the alpha 2-adrenergic receptors in the iris-ciliary body, which reduces the intracellular cAMP level, is stronger than that via the beta-adrenergic receptors.
authors.affiliation: Department of Ophthalmology, University of California at San Diego, La Jolla 92093-0946, USA.
authors.forename: J H
authors.initials: JH
authors.lastname: Liu
authors.forename: J
authors.initials: J
authors.lastname: Gallar
mesh_terms: D000287:Administration, Topical; D000316:Adrenergic alpha-Agonists / Q000008:administration & dosage*; D000317:Adrenergic alpha-Antagonists / Q000008:administration & dosage; D000319:Adrenergic beta-Antagonists / Q000008:administration & dosage; D000818:Animals; D001082:Aqueous Humor / Q000187:drug effects / Q000378:metabolism; D002924:Ciliary Body / Q000187:drug effects / Q000378:metabolism* / Q000601:surgery; D000242:Cyclic AMP / Q000378:metabolism*; D015232:Dinoprostone / Q000378:metabolism; D004195:Disease Models, Animal; D004359:Drug Therapy, Combination; D004837:Epinephrine / Q000008:administration & dosage*; D005901:Glaucoma / Q000188:drug therapy / Q000378:metabolism / Q000503:physiopathology; D007429:Intraocular Pressure / Q000187:drug effects; D007498:Iris / Q000187:drug effects / Q000378:metabolism* / Q000601:surgery; D017075:Laser Coagulation / Q000009:adverse effects; D009883:Ophthalmic Solutions; D011817:Rabbits; D011863:Radioimmunoassay; D013999:Timolol / Q000008:administration & dosage; D015016:Yohimbine / Q000008:administration & dosage
chemical_list: D000316:Adrenergic alpha-Agonists; D000317:Adrenergic alpha-Antagonists; D000319:Adrenergic beta-Antagonists; D009883:Ophthalmic Solutions; D015016:Yohimbine; D013999:Timolol; D000242:Cyclic AMP; D015232:Dinoprostone; D004837:Epinephrine