title: Dopamine modulation of active ion transport in rabbit corneal epithelium.
abstract: The addition of micromolar quantities of dopamine stimulated ion transport in the isolated rabbit corneal epithelium. This response was blocked by pretreatment with the dopamine antagonist, haloperidol, and by the elimination of Cl- from the bathing solutions. The beta-adrenergic antagonist, timolol, was also a potent inhibitor of the epithelial response to dopamine. The presence of the serotonin antagonist, methysergide, or the dopamine beta-hydroxylase inhibitor, FLA-63, did not significantly alter the corneal response to dopamine. Following superior cervical ganglionectomy, the epithelial response to dopamine was abolished. These findings are consistent with the idea that Cl- secretion in the rabbit corneal epithelium can be modulated by preterminal dopamine receptors located on the sympathetic nerve fibers; therefore, dopamine stimulation appears to be a serial process mediated by the release of norepinephrine from sympathetic nerve terminals in the epithelium.
mesh_terms: D000818:Animals; D001693:Biological Transport, Active; D005406:Bis(4-Methyl-1-Homopiperazinylthiocarbonyl)disulfide / Q000494:pharmacology; D002069:Butaclamol / Q000494:pharmacology; D002712:Chlorides / Q000378:metabolism* / Q000494:pharmacology; D003315:Cornea / Q000378:metabolism*; D004298:Dopamine / Q000502:physiology*; D004553:Electric Conductivity; D004848:Epithelium / Q000378:metabolism; D006220:Haloperidol / Q000494:pharmacology; D011817:Rabbits; D013562:Sympathectomy; D013999:Timolol / Q000494:pharmacology
chemical_list: D002712:Chlorides; D005406:Bis(4-Methyl-1-Homopiperazinylthiocarbonyl)disulfide; D013999:Timolol; D002069:Butaclamol; D006220:Haloperidol; D004298:Dopamine