Localization of Vasodilator Dopamine Receptors in the Canine Hindlimb

Abstract

1 Vascular responses to local injection of dopamine and isoprenaline have been compared in the blood-perfused gracilis muscle and hind paw pads of dogs anaesthetized with chloralose.2 In the paw pads, dopamine (0.5 to 5.0 gg) caused a transient vasoconstriction followed by dosedependent vasodilatation. a-Adrenoceptor blockade converted this response to pure vasodilatation, which was attenuated or abolished by the dopamine-receptor antagonist, haloperidol (1 to 2mg i.a.). In the gracilis, dopamine produced only vasoconstriction. Following a-adrenoceptor blockade this was abolished, but only a very small dilator response was revealed. 3 Isoprenaline (0.05 to 0.5 jig) caused dose-dependent dilatation in both beds, which was attenuated by propranolol (0.1 mg/kg i.v.).4 Glyceryl trinitrate (0.2 to 5.0 gg) was used to assess vascular reactivity. When responses to isoprenaline and dopamine were compared with those to glvceryl trinitrate, both beds had approximately equal reactivity to isoprenaline. In contrast the paw pads were 10 fold more responsive to dopamine than was the gracilis. 5 We conclude that the vessels of the paw pads play an important part in the femoral dilator response to dopamine.

Evidence for Dopaminergic Vasodilator Innervation of the Canine Paw Pad

“…Its effect is therefore compatible with the concept that the transmitter liberated by the dilator axons in the tibial nerve is dopamine or a related substance. Such a view is consistent with the observation that the majority of femoral dopamine receptors are localized in the vasculature of the paw pad (Bell & Stubbs, 1978). It is also supported by histochemical and biochemical data which indicate that the arteriovenous anastomoses of the paw pads are innervated by a population of non-adrenergic axons containing high levels of dopamine (Bell, Lang & Laska, 1978a).…”

“…The canine femoral vascular bed is known to contain vasodilator receptors for dopamine which are distinct from fJ-adrenoceptors (Bell, Conway, Lang & Padanyi, 1975), and recently it has been demonstrated 0007-1 188/79/I 10337-07 S01.00 that these dopamine receptors are localized predominantly within the vasculature of the paw pads (Bell & Stubbs, 1978). It was therefore of interest to determine whether the pharmacological characteristics of the atropine-and antihistamine-resistant neurogenic dilator response in the paw are consistent with its mediation by dopamine.…”

Pharmacological investigations of the vasodilator nerves supplying the duck's foot

“…The present results show that the vasculature of the duck foot is highly responsive to dopamine, profound reductions of vascular tone being produced by quite small amounts of dopamine in the absence of pharmacological procedures for inactivation of oaadrenoceptors. By contrast, in the mammalian foot dopamine-induced dilatation is not pronounced unless the concomitant constrictor effect of dopamine on x-adrenoceptors is first abolished with an appropriate drug (Bell & Stubbs, 1978). We observed no dilator effect of isoprenaline in doses as high as 1.2 ytmol, suggesting the absence of appreciable numbers of ,B-adrenoceptors in the foot.…”

Heat conservation during cold exposure in birds (vasomotor and respiratory implications)

“…His studies leave open the possibility of a purinergic type innervation. Hillman et al (1982) also excluded that the active vasodilatation in the chicken is due to dopaminergic neurons such as suggested for AVA dilatation in the dog hindlimb (Bell & Stubbs 1978).…”