Sympathetic vasoconstriction in the rat anterior choroid is mediated by alpha1-adrenoceptors

These experiments were undertaken in an attempt to use laser-Doppler flowmetry to measure anterior choroidal blood flow in the anesthetized rat and to study the mechanism by which sympathetic nerve stimulation might produce vasoconstriction in this vascular bed. Electrical stimulation of the preganglionic cervical sympathetic nerve produced reproducible, frequency-related ocular vasoconstrictor responses with maximal vasoconstriction seen at about 32 Hz. Ocular vasoconstrictor responses were blocked by intravenous treatment with the nonselective alpha-adrenoceptor antagonists, phentolamine (5 mg kg(-1)) and phenoxybenzamine (2 mg kg(-1)), as well as with the selective alpha1-adrenoceptor antagonist, prazosin (0.3 mg kg(-1)). In contrast, the selective alpha2-adrenoceptor blocker, rauwolscine (0.5 mg kg(-1)), only potentiated the vasoconstriction. Neither intravenous atropine (1 mg kg(-1)) nor propranolol (1 mg kg(-1)) altered the magnitude of neurally evoked vasoconstriction. These results demonstrate the usefulness of laser-Doppler flowmetry in studies of the rat anterior choroidal circulation and suggest that adrenergic neurogenic vasoconstriction in the anterior segment of the rat eye is mediated almost exclusively by alpha1-adrenoceptor mechanisms.