Abstract

Electrical stimulation of the preganglionic cervical sympathetic nerve produced ocular vasoconstrictor responses as measured from the anterior choroid of anesthetized cats using laser-Doppler flowmetry. Ipsilateral nictitating membrane contractions were simultaneously measured as an established index of neural sympathetic activation. The frequency-response relationships for both effectors were nearly linear from 0·125-32 Hz. When elicited at 2-min intervals, submaximal evoked responses of both systems were stable for more than 1 hr. Ocular vasoconstrictor and nictitating membrane responses were blocked in a dose-dependent fashion by intravenous treatment with the non-selective α-adrenoceptor antagonist phentolamine (0·1-3·0 mg kg-1) and with phenoxybenzamine (3·0 mg kg-1) as well as with the selective α1-adrenoceptor antagonist, prazosin (10-300 μg kg-1). In contrast, neither evoked response was antagonized by α2-adrenoceptor blocker, yohimbine (10-300 μg kg-1), nor with rauwolscine (500 μg kg-1). No significant alteration in magnitude of ocular vasoconstriction was seen with blockade of either muscarinic (atropine, 1 mg kg-1) or β-adrenergic (propranolol, 1 mg kg-1) receptors. These results demonstrate the usefulness of laser-Doppler flowmetry in studies of the choroidal circulation and suggest that, as previously established for the nictitating membrane, adrenergic neurogenic vasoconstriction in the anterior segment of the eye is mediated almost exclusively by α1-adrenoceptor mechanisms.

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