The study suggests that adrenaline-induced vasodilatation in skeletal muscle is primarily mediated by reflex nervous mechanisms rather than a functional isoprenaline-like metabolite.
Challenges metabolite mediation of adrenaline vasodilatation; leaves open reflex mechanisms for human validation.
A depressor substance, which resembled isoprenaline in Rf value, was demonstrated after chromatography of plasma collected from chloralose-anaesthetised cats during the blood pressure responses to intravenous injections of adrenaline, but the results obtained did not substantiate the hypothesis of a functional metabolite. The amount of vasodilatation that the “metabolite” would have caused in the skeletal muscles of the hind limb could not, for example, be correlated with the increases in blood flow produced by the original intravenous doses of adrenaline. The fact that adrenaline was largely vasoconstrictor in acutely denervated hind limbs was taken to indicate that the original vasodilator effects were of reflex nervous origin. It is suggested that the afferent source of this and related reflexes involves the stimulation of chemoreceptors as opposed to mechanoreceptors and that increases in flow through denervated muscles in response to adrenaline are caused by a direct action on the walls of the blood vessels.
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David J. Roberts (1965) studied this question.
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