title: Sympathetic stimulation elicits increased or decreased VO2 in the perfused rat hindlimb via alpha 1-adrenoceptors.
abstract: The effects of lumbar sympathetic nerve stimulation on oxygen uptake (VO2) 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 VO2 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 VO2 were almost completely blocked by the alpha 1/alpha 2-blocker phentolamine (1.0 microM) but were not affected by the beta 1/beta 2-blocker DL-propranolol (2.0 microM). The alpha 2-blocker yohimbine (0.1 microM) did not significantly affect either the pressor or VO2 response. The alpha 1-antagonist prazosin (0.1 microM) abolished the vasoconstriction with low-frequency stimulation and inhibited > 90% of the vasoconstriction with high-frequency stimulation. Intra-arterial infusion of phenylephrine (alpha 1-agonist), but not of UK-14304 (alpha 2-agonist), also elicited a similar biphasic response in VO2 during vasoconstriction. The changes in VO2 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 VO2 and vasoconstriction. Thus sympathetic control of VO2 in the perfused rat hindlimb appears to be initiated by activation of predominantly vascular alpha 1-adrenoceptors.
authors.affiliation: Division of Biochemistry, University of Tasmania, Hobart, Australia.
authors.forename: J L
authors.initials: JL
authors.lastname: Hall
authors.forename: J M
authors.initials: JM
authors.lastname: Ye
authors.forename: M G
authors.initials: MG
authors.lastname: Clark
authors.forename: E Q
authors.initials: EQ
authors.lastname: Colquhoun
mesh_terms: D058646:Adrenergic alpha-1 Receptor Agonists; D058668:Adrenergic alpha-1 Receptor Antagonists; D058647:Adrenergic alpha-2 Receptor Agonists; D058669:Adrenergic alpha-2 Receptor Antagonists; D000316:Adrenergic alpha-Agonists / Q000494:pharmacology; D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000818:Animals; D004305:Dose-Response Relationship, Drug; D004558:Electric Stimulation; D006614:Hindlimb / Q000098:blood supply*; D008297:Male; D010101:Oxygen Consumption; D051381:Rats; D017208:Rats, Wistar; D018340:Receptors, Adrenergic, alpha-1 / Q000502:physiology*; D018341:Receptors, Adrenergic, alpha-2 / Q000502:physiology; D014661:Vasoconstriction / Q000187:drug effects
chemical_list: D058646:Adrenergic alpha-1 Receptor Agonists; D058668:Adrenergic alpha-1 Receptor Antagonists; D058647:Adrenergic alpha-2 Receptor Agonists; D058669:Adrenergic alpha-2 Receptor Antagonists; D000316:Adrenergic alpha-Agonists; D000317:Adrenergic alpha-Antagonists; D018340:Receptors, Adrenergic, alpha-1; D018341:Receptors, Adrenergic, alpha-2