SUMMARY Using stereotaxic procedures, we electrically stimulated specific sites in the hypothalamus and midbrain of anesthetized dogs pretreated with guanethidine and atropine methonitrate. A tract in which stimulation caused noncholinergic dilator responses in the hindlimbs was identified. The course of this trace was different from that subserving cholinergic vasodilation in the hindlimb musculature. In a number of experiments we studied the proportional distribution of blood flow to leg and paw. Responses restricted to the paw were regarded as occurring mainly in cutaneous vessels; those restricted to the leg were regarded as occurring mainly in the skeletal muscle vessels. Some dilator responses in both beds were abolished by intra-arterial administration of antihistamines: other dilator responses were abolished by intra-arterial injections of dopamine antagonists. Centrally evoked dilation of leg and paw vessels by noncholinergic pathways suggests physiological roles for these fibers in the regulation of cardiovascular function.CHOLINERGIC sympathetic vasodilator fibers supplying the vascular bed of the hindlimb musculature in the dog and the cat first were demonstrated by Bulbring and Burn 1 and subsequently their central projections through the hypothalamus were described by Eliasson et al. 2 and Abrahams et al. 3 In both species, peripheral stimulation of the sympathetic nervous system when the effects of acetylcholine are abolished by atropine still can produce dilation of the vascular bed of the hindlimb. 4 ' 8 This dilation occurs in both muscle and skin and is partly sensitive and partly resistant to the action of antihistaminic agents. Studies employing electrical stimulation of the medulla also have provided evidence for dilator responses in the hindlimb that cannot be attributed to activation of sympathetic cholinergic fibers.9 -'° In a preliminary report, Bell et a l . " demonstrated that electrical stimulation at specific loci in the hypothalamus and midbrain of the dog can evoke noncholinergic dilations in the hindlimb. Our present study has extended these findings to investigate the distribution of the noncholinergic dilator nerves between leg and paw and to obtain pharmacological evidence for the peripheral transmitters involved. MethodsMongrel dogs of either sex and weighing 12-22 kg were anesthetized with chloralose (70 mg/kg, iv) after induction with thiopental (thiopentone) sodium. Supplemental doses of chloralose were administered during the experiment to maintain constant anesthesia, and all dogs were artificially ventilated. Blood flow in one or both femoral arteries was recorded by cuff-type electromagnetic flow probes and a Devices flow meter. Systemic blood pressure was recorded from a branch of the right femoral artery with a Beckman pressure transducer, and heart rate was re- corded from standard electrocardiographic limb leads integrated through a cardiotachometer coupler. Results were recorded on a four-channel Beckman R 411 Dynograph recorder. All dogs were treated with guaneth...
Increases in femoral blood flow were produced by intra-arterial injections of dopamine (5-50 Sg) in some but not all anaesthetized dogs studied, following treatment with the ca-adrenoceptor antagonist, phentolamine. 2 The dilator effect of dopamine was not due to inhibition of adrenergic vasomotor tone as it was not affected by pharmacological procedures which completely abolished the activity of vasomotor nerves.3 Blockade of vascular j-adrenoceptors using propranolol reduced the flow increases produced by dopamine much less than it did those produced by isoprenaline. 4 Responses to dopamine were significantly depressed by intra-arterial administration of ergometrine (0.5 mg). This dose of ergometrine did not reduce femoral dilator responses to acetylcholine, histamine, isoprenaline, bradykinin or 5-hydroxytryptamine. 5 It is concluded that the femoral vascular bed in the dog contains specific vasodilator receptors for dopamine. Ergometrine appears to be a selective antagonist of dopamine at these receptors.
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