title: Skeletal muscle vasodilatation during sympathoexcitation is not neurally mediated in humans.
abstract: Evidence for the existence of sympathetic vasodilator nerves in human skeletal muscle is controversial. Manoeuvres such as contralateral ischaemic handgripping to fatigue that cause vasoconstriction in the resting forearm evoke vasodilatation after local alpha-adrenergic receptor blockade, raising the possibility that both constrictor and dilator fibres are present. The purpose of this study was to determine whether this dilatation is neurally mediated. Ten subjects (3 women, 7 men) performed ischaemic handgripping to fatigue before and after acute local anaesthetic block of the sympathetic nerves (stellate ganglion) innervating the contralateral (resting) upper extremity. Forearm blood flow was measured with venous occlusion plethysmography in the resting forearm. In control studies there was forearm vasoconstriction during contralateral handgripping to fatigue. During contralateral handgripping after stellate block, blood flow in the resting forearm increased from 6.1 +/- 0.7 to 18.7 +/- 2.2 ml dl-1 min-1 (P < 0.05). Mean arterial pressure measured concurrently increased from approximately 90 to 130 mmHg and estimated vascular conductance rose from 6.5 +/- 0.7 to 14.0 +/- 1.5 units, indicating that most of the rise in forearm blood flow was due to vasodilatation. Brachial artery administration of beta-blockers (propranolol) and the nitric oxide (NO) synthase inhibitor N G-monomethyl-L-arginine (L-NMMA) after stellate block virtually eliminated all of the vasodilatation to contralateral handgrip. Since vasodilatation was seen after stellate block, our data suggest that sympathetic dilator nerves are not responsible for limb vasodilatation seen during sympathoexcitation evoked by contralateral ischaemic handgripping to fatigue. The results obtained with propranolol and L-NMMA suggest that beta-adrenergic mechanisms and local NO release contribute to the dilatation.
authors.affiliation: Mayo Medical School and Departments of Physiology and Anesthesiology, Mayo Clinic and Foundation, Rochester, MN 55905, USA.
authors.forename: A S
authors.initials: AS
authors.lastname: Reed
authors.forename: M E
authors.initials: ME
authors.lastname: Tschakovsky
authors.forename: C T
authors.initials: CT
authors.lastname: Minson
authors.forename: J R
authors.initials: JR
authors.lastname: Halliwill
authors.forename: K D
authors.initials: KD
authors.lastname: Torp
authors.forename: L A
authors.initials: LA
authors.lastname: Nauss
authors.forename: M J
authors.initials: MJ
authors.lastname: Joyner
mesh_terms: D000293:Adolescent; D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000328:Adult; D001794:Blood Pressure; D004837:Epinephrine / Q000097:blood; D005260:Female; D005542:Forearm; D006225:Hand; D006801:Humans; D008297:Male; D018763:Muscle Fatigue; D018482:Muscle, Skeletal / Q000098:blood supply / Q000294:innervation / Q000502:physiology*; D009569:Nitric Oxide / Q000378:metabolism; D010991:Plethysmography; D011433:Propranolol / Q000494:pharmacology; D012039:Regional Blood Flow; D013233:Stellate Ganglion / Q000187:drug effects; D013564:Sympathetic Nervous System / Q000187:drug effects / Q000502:physiology*; D014661:Vasoconstriction / Q000187:drug effects / Q000502:physiology; D014664:Vasodilation / Q000187:drug effects / Q000502:physiology*; D019323:omega-N-Methylarginine / Q000494:pharmacology
chemical_list: D000319:Adrenergic beta-Antagonists; D019323:omega-N-Methylarginine; D009569:Nitric Oxide; D011433:Propranolol; D004837:Epinephrine