title: Age- and limb-related differences in the vasoconstrictor response to limb dependency are not mediated by a sympathetic mechanism in humans.
abstract: OBJECTIVE
  We tested the hypotheses that vasoconstrictor responses to limb dependency are: (i) greater in the leg than the arm, (ii) impaired with age and (iii) not sympathetically mediated.
  
  
  METHODS
  Vascular responses to limb dependency (i.e. lowering the limb from heart level to 30 cm below heart level) were determined in 17 young and 17 older adults. Indices of blood flow were obtained in the brachial and popliteal arteries (Doppler ultrasound) as well as in the cutaneous circulation (forearm and calf using laser-Doppler flowmetry). Vasoconstriction was quantified by calculating the indices of vascular resistance as height corrected mean arterial pressure/limb blood velocity or skin flux. A second group of subjects repeated the limb dependency trials after acute systemic sympathetic blockade.
  
  
  RESULTS
  Limb dependency increased vascular resistance index in the brachial artery (∆59 ± 8%; P<0.05) and popliteal artery (∆99 ± 10%; P<0.05 for change in heart level and brachial vs. popliteal) of young and older adults (∆60 + 9% brachial and ∆61 ± 7% popliteal arteries; P<0.05 for change in heart level and response in popliteal young vs. older adults). In contrast, cutaneous vasoconstrictor responses to limb dependency were similar in the forearm (∆218 ± 29% and ∆200 ± 29% for young and older adults, respectively) and calf (∆257 ± 32% and ∆236 ± 29%; all P<0.05 from heart level) of young and older adults. Vasoconstrictor responses to limb dependency were not affected by sympathetic blockade in young or older adults.
  
  
  CONCLUSIONS
  These findings indicate that age-, limb-, and tissue-related differences may exist in the vasoconstrictor response to limb dependency in healthy humans, which are not sympathetically mediated.
authors.affiliation: Penn State Heart and Vascular Institute, Pennsylvania State University College of Medicine, Hershey, PA 17033-2390, USA.
authors.forename: K A M
authors.initials: KA
authors.lastname: Snyder
authors.forename: S
authors.initials: S
authors.lastname: Shamimi-Noori
authors.forename: T E
authors.initials: TE
authors.lastname: Wilson
authors.forename: K D
authors.initials: KD
authors.lastname: Monahan
mesh_terms: D018674:Adrenergic Antagonists / Q000494:pharmacology; D000328:Adult; D000368:Aged; D000375:Aging / Q000502:physiology*; D001132:Arm / Q000098:blood supply* / Q000294:innervation*; D001794:Blood Pressure / Q000502:physiology; D001916:Brachial Artery / Q000502:physiology; D005260:Female; D006339:Heart Rate / Q000502:physiology; D006801:Humans; D007866:Leg / Q000098:blood supply* / Q000294:innervation*; D008297:Male; D008875:Middle Aged; D010646:Phentolamine / Q000494:pharmacology; D011150:Popliteal Artery / Q000502:physiology; D011433:Propranolol / Q000494:pharmacology; D012039:Regional Blood Flow / Q000502:physiology; D013564:Sympathetic Nervous System / Q000187:drug effects / Q000502:physiology*; D014655:Vascular Resistance / Q000502:physiology; D014661:Vasoconstriction / Q000502:physiology*
chemical_list: D018674:Adrenergic Antagonists; D011433:Propranolol; D010646:Phentolamine