Sympathetic stimulation elicits increased or decreased V̇O₂ in the perfused rat hindlimb via α₁-adrenoceptors

The effects of lumbar sympathetic nerve stimulation on oxygen uptake (V̇O₂) in curarized muscle of the perfused rat hindlimb were investigated. Stimulation of sympathetic nerves elicited vasoconstriction at all frequencies. Importantly, this was associated with changes in V̇O₂ that were generally stimulatory at low frequencies (0.5-2 Hz) and inhibitory at high frequencies (5-10 Hz). Both the pressor response and the changes in V̇O₂ were almost completely blocked by the α₁/α₂-blocker phentolamine (1.0 μM) but were not affected by the β₁/β₂-blocker DL-propranolol (2.0 μM). The α₂-blocker yohimbine (0.1 μM) did not significantly affect either the pressor or V̇O₂ response. The α₁-antagonist prazosin (0.1 μM) abolished the vasoconstriction with low frequency stimulation and inhibited >90% of the vasoconstriction with high-frequency stimulation. Intra-arterial infusion of phenylephrine (α₁-agonist), but not of UK-14304 (α₂-agonist), also elicited a similar biphasic response in V̇O₂ during vasoconstriction. The changes in V̇O₂ at both low- and high-frequency stimulation were fully reversed by prazosin. The vasodilator sodium nitroprusside also showed similar effects to prazosin in blocking both. V̇O₂ and vasoconstriction. Thus sympathetic control of V̇O₂ in the perfused rat hindlimb appears to be initiated by activation of predominantly vascular α₁-adrenoceptors.