Sympathetic stimulation elicits increased or decreased Vc>2 in the perfused rat hindlimb via α1-adrenoceptors

The effects of lumbar sympa-thetic nerve stimulation on oxygen uptake (Vu2) 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 Vc>2 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 V02 were almost completely blocked by the o/c-blocker phentolamine (1.0 M) but were not affected by the i/2-blocker DL-propranolol (2.0 #M). The 02-blocker yohimbine (0.1 M) did not significantly affect either the pressor or Vc>2 response. The ai-aritagonist prazosin (0.1 ;/M) abolished the vasoconstriction with lowfrequency stimulation and inhibited >90% of the vasoconstriction with high-frequency stimulation. Intra-arterial infusion of phenylephrine (i-agonist), but not of UK-14304 (a2agonist), also elicited a similar biphasic response 'in Vo2 during vasoconstriction. The changes in Vc>2 at both low- and high-frequency stimulation were fully reversed by prazosin. The vasodilator sodium niroprusside, also showed similar effects to prazosin in blocking both VO2 and vasoconstriction. Thus sympathetic control of Vc>2 in the perfused rat hindlimb appears to be initiated by activation of predominantly vascular o-adrenoceptors. oxygen uptake; vasoconstriction; vascular control; nutritive flow; nonnutritive flow; adrenergic antagonists; adrenergic agonists