Postsynaptic alpha 1- and alpha 2-adrenoceptors in the vascular system of the herring gull, Larus argentatus.

The nature of the vascular alpha-adrenoceptors has been studied in the herring gull, Larus argentatus. In the anaesthetized herring gull, both phenylephrine and clonidine elicited dose-dependent increases in arterial blood pressure. The alpha 1-adrenoceptor antagonist prazosin was a better antagonist of phenylephrine than were the alpha 2-adrenoceptor antagonists yohimbine and rauwolscine. Yohimbine and rauwolscine were better antagonists of clonidine than was prazosin. The maximum response to phenylephrine, but not clonidine, was lower in reserpine-treated birds, indicating that phenylephrine in high doses liberates endogenous catecholamines, which contribute to the effect. It is concluded that the herring gull possesses postsynaptic, vascular alpha-adrenoceptors, of both the alpha 1- and alpha 2-subtypes, similar to those found in mammals.

Cardiovascular and biochemical effects of L-DOPA in the sea-gull, Larus argentatus.

We have investigated the effects of L-DOPA alone and in combination with three different inhibitors of L-aromatic aminoacid decarboxylase (DC), carbidopa, benserazid and alpha-monofluoromethyldopa (MFMD) on blood pressure (BP) and catecholamine content in conscious or anaesthetized sea-gulls, Larus argentatus. The results show that L-DOPA, given i.p., is taken up and decarboxylated to dopamine (DA) in brain and heart. Carbidopa inhibits the peripheral synthesis of DA from exogenous L-DOPA while central decarboxylation is enhanced when compared to the effects of L-DOPA alone. Benserazid and MFMD inhibit both central and peripheral formation of DA after L-DOPA injections. L-DOPA given alone leads to a slight increase in BP, while heart rate (HR) decreases somewhat. After peripheral inhibition of DC using carbidopa, L-DOPA elicits a reduction in BP both in conscious and anaesthetized birds. HR is significantly reduced in anaesthetized birds. Pretreatment with benserazid or MFMD abolishes the cardiovascular effects of L-DOPA. It is concluded that L-DOPA lowers the BP via activation of central mechanisms.

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.

Cardiovascular effects of clonidine in an avian species, Larus argentatus.

Blood pressure and heart rate were recorded in the sea gull, Larus argentatus, under light pentibarbitone anaesthesia. Clonidine 10(-7) and 10(-8) mol . kg-1 (27 and 2.7 microgram . kg-1) i.v. produced a biphasic effect on blood pressure, a brief initial increase being followed by a prolonged hypotensive response. There was an immediate reduction in heart rate rate which persisted throughout the hypotensive phase. After spinal transection at the level of C4, clonidine administration elicited hypertension and bradycardia. Bilateral vagotomy abolished the effect of clonidine on heart rate but did not alter the blood pressure response. Vagotomy in combination with spinal transection abolished the effect of clonidine on heart rate but the hypertensive response was accentuated. Yohimbine 10(-7) or 10(-6) mol . kg-1 (0.039 or 0.39 mg . kg-1) given 5 min after clonidine 10(-7) mol.kg-1 (27 microgram . kg-1) effectively antagonized the cardiovascular effects of clonidine, while prazosin 10(-7) or 10(-6) mol . kg (0.042 or 0.42 mg . kg-1) had no such effect. We conclude that clonidine acts in the central nervous system of the sea gull to produce a lowering of blood pressure and heart rate. These effects are mediated by central inhibition of sympathetic activity and, in the case of the heart rate, mostly by central activation of vagal activity to the heart. This central action of clonidine involves activation of alpha-adrenoceptors which are blocked by yohimbine but not by prazosin and therefore may belong to the alpha 2 subtype.