Mediation and mechanisms of the hypotensive effect of L-dopa in the sea-gull: Larus argentatus.

We have investigated the mediation of the hypotensive action of L-DOPA after peripheral DOPA decarboxylase (DC) inhibition in the sea-gull, Larus argentatus. Vagotomy prevented the bradycardia and hypotension occurring after L-DOPA in birds pretreated with an inhibitor of peripheral DC. L-DOPA alone, given to intact birds, resulted in a slight increase in blood pressure (BP), accompanied by a tendency to bradycardia. Spinal transection in combination with vagotomy reversed the bradycardia and reinforced the increase in BP seen in intact birds after L-DOPA. The dopamine receptor antagonist spiroperidol did not alter the hypotension and bradycardia after L-DOPA in birds pretreated with a peripherally acting DC inhibitor. Yohimbine antagonized the effects of L-DOPA, restoring the BP to near basal values within 5 min after i.v. injections, while prazosin had no such effect. The heart rate returned towards basal values after both yohimbine and prazosin. We conclude that L-DOPA elicits its hypotensive action in the sea-gull via activation of central alpha-adrenoceptors, which may belong to the alpha 2-subtype. The bradycardia may involve central activation of adrenoceptors of both the alpha 1- and alpha 2-types. The hypotension and bradycardia are mediated via vagal activation and probably also inhibition of sympathetic nervous output. The functional significance of sympathetic fibres running along with the vagus nerve is suggested.