SYMPATHETIC-STIMULATION ELICITS INCREASED OR DECREASED VO2 IN THE PERFUSED RAT HINDLIMB VIA ALPHA(1)-ADRENOCEPTORS

The effects of lumbar sympathetic nerve stimulation on oxygen uptake ( (V) over dot O-2) in curarized muscle of the perfused rat hindlimb wer e investigated. Stimulation of sympathetic nerves elicited vasoconstri ction at all frequencies. Importantly, this was associated with change s in (V) over dot O-2 that were generally stimulatory at low frequenci es (0.5-2 Hz) and inhibitory at high frequencies (5-10 Hz). Both the p resser response and the changes in (V) over dot O-2 were almost comple tely blocked by the alpha(1)/alpha(2)-blocker phentolamine (1.0 mu M) but were not affected by the beta(1)/beta(2)-blocker DL-propranolol (2 .0 mu M). The alpha(2)-blocker yohimbine (0.1 mu M) did not significan tly affect either the presser or (V) over dot O-2 response. The al-ant agonist prazosin (0.1 mu M) abolished the vasoconstriction with low-fr equency stimulation and inhibited > 90% of the vasoconstriction with h igh-frequency stimulation. Intra-arterial infusion of phenylephrine (a lpha(1)-agonist), but not of UK-14304 (alpha(2)-agonist), also elicite d a similar biphasic response in VO2 during vasoconstriction. The chan ges in (V) over dot O-2 at both low- and high-frequency stimulation we re fully reversed by prazosin. The vasodilator sodium nitroprusside al so showed similar effects to prazosin in blocking both (V) over dot O- 2 and vasoconstriction. Thus sympathetic control of (V) over dot O-2 i n the perfused rat hindlimb appears to be initiated by activation of p redominantly vascular alpha(1)-adrenoceptors.