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Cutaneous Active Vasodilation is Not Abolished by Atropine in Cystic Fibrosis
Author(s) -
Kellogg Dean Lundt,
Orozco Carlos Raul,
Phillips Teresa Marie,
Alvarez Guy,
Zhao Joan Liu,
Johnson John Marshall
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.5.a1400-a
To test the hypothesis that cutaneous active vasodilation(AVD) in heat stress is mediated by a redundant acetylcholine(Ach)‐VIP cotransmitter system, we examined the effects of atropine(ATR) on AVD in persons with(CF) and without cystic fibrosis (non‐CF). VIP‐containing cutaneous neurons are sparse in CF, yet AVD during heat stress is normal. In CF, the AVD cotransmitter system could compensate for deficient VIP by augmented Ach release; if so, AVD in CF would be abolished by ATR. ATR was administered into skin by iontophoresis in 5 CF and 5 matched non‐CF. Skin blood flow was monitored by laser Doppler flowmetry(LDF) at ATR treated and untreated sites. Blood pressure(MAP) was monitored(Finapres) and cutaneous vascular conductance calculated. The protocol began with a normothermic period followed by 30–45 minutes of heat stress. Subjects were then cooled and LDF sites warmed to 42°C to effect maximal vasodilation. CVC's were normalized to these maxima. During heat stress in CF, CVC increased from 12±2%max to 60±8%max(p<0.05) at untreated sites and from 11±2%max to 42±7%max(p<0.05) at ATR sites. During heat stress in non‐CF, CVC increased from 10±0%max to 48±5%max(p<0.05) at untreated sites, and from 14±3%max to 38±3%max(p<0.05) at ATR sites. ATR attenuated CVC increases in CF and non‐CF(p<0.05). ATR's effect did not differ between groups(p>0.05), thus CF does not depend on Ach for AVD. The failure of ATR to abolish AVD in CF, suggests involvement of multiple cotransmitters or that CF patients are highly sensitive to the sparse VIP present in their skin.( HL065599 , HL059166 )