Abstract

Dopamine, injected into the lumbar aorta of the dog in doses which produce a reversible inhibition of synaptic transmission in the lumbar paravertebral ganglia (0.5-64x10-8 moles), produces a neurogenic vasodilatation in the isolated perfused hindleg or gracilis muscle. This was abolished by acute preganglionic decentralization and by administration into the perfused preparation of alpha-adrenoceptor blocking agents, but not of atropine or diphenhydramine. After decentralization, preganglionic electrical stimulation restored the dopamine-induced indirect vasodilatation. The neurogenic vasodilatation was also seen with intra-aortic injections of epinine (2-32x10-8 moles) and apomorphine (1.2-19.2x10-8 moles) and was preferentially blocked by haloperidol (0.26x10-6 moles). (-)-Noradrenaline, injected into the lumbar aorta in baroreceptor-denervated dogs, was found to be equipotent with dopamine in eliciting the neurogenic vasodilatation; this (-)-noradrenaline-induced effect was preferentially blocked by phentolamine (8x10-6 moles). The possibility that the neurogenic vasodilatation, which occurs upon intra-aortic injection of dopamine in the dog, is due to its gnaglionic-inhibitory effect is discussed.

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