title: High-salt diet increases hormonal sensitivity in skin pre-capillary resistance vessels.
abstract: OBJECTIVE
  Recent data indicate that the skin of rats on a high-salt diet is able to accumulate Na(+) without commensurate water. This extrarenal mechanism of Na(+) homoeostasis could affect skin vasoregulation. We hypothesized that the major resistance vessel of rat skin, the pre-capillary arterioles, has increased vasoreactivity within the physiological range of circulating ANG II, a hormone relevant to salt-sensitive hypertension.
  
  
  RESULTS
  Skin arterioles from skin and muscle were isolated using the agar-infusion technique. Vessels from rats fed high-salt and low-salt diet had similar lumen diameter and media area/lumen area ratio. Contractile sensitivity to ANG II was increased in skin vessels from high-salt vessels at all doses tested starting at 10(-10) m (P < 0.01). Pre-capillary arterioles from muscle displayed similar contractions to ANG II, independent of the diet. As ANG II and the renin-angiotensin system are strongly involved in salt conservation, we explored whether vasoreactivity for noradrenaline was increased as well, because this is a functionally unrelated hormone. At low doses, contractions were similar, but at 10(-5) and 10(-4) m, noradrenaline produced stronger contractions in skin vessels from high-salt compared with low-salt rats (P < 0.01).
  
  
  CONCLUSIONS
  Our data demonstrate significantly increased hormonal vasoreactivity of skin vessels from rats on a high-salt diet, which could increase peripheral resistance in many situations and contribute to higher pressure in salt-sensitive hypertension. As vessels from adjacent muscle were unaffected, we raise the interesting possibility that increased vasoreactivity in the skin could be linked to osmotically inactive Na(+) accumulation.
authors.affiliation: Renal Research Group, Institute of Medicine, University of Bergen, Bergen, Norway; Department of Medicine, Haukeland University Hospital, Bergen, Norway. Frank.Helle@med.uib.no
authors.forename: F
authors.initials: F
authors.lastname: Helle
authors.forename: T V
authors.initials: TV
authors.lastname: Karlsen
authors.forename: O
authors.initials: O
authors.lastname: Tenstad
authors.forename: J
authors.initials: J
authors.lastname: Titze
authors.forename: H
authors.initials: H
authors.lastname: Wiig
mesh_terms: D000804:Angiotensin II / Q000494:pharmacology*; D000818:Animals; D001160:Arterioles / Q000187:drug effects / Q000378:metabolism; D004039:Diet, Sodium-Restricted; D004305:Dose-Response Relationship, Drug; D008297:Male; D009638:Norepinephrine / Q000494:pharmacology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012867:Skin / Q000098:blood supply*; D017673:Sodium Chloride, Dietary / Q000008:administration & dosage / Q000378:metabolism*; D014655:Vascular Resistance / Q000187:drug effects*; D014661:Vasoconstriction / Q000187:drug effects*; D014662:Vasoconstrictor Agents / Q000494:pharmacology*
chemical_list: D017673:Sodium Chloride, Dietary; D014662:Vasoconstrictor Agents; D000804:Angiotensin II; D009638:Norepinephrine