Submitted on March 12, 2007
Accepted on June 25, 2007
Cholinergic Mechanisms of Cutaneous Active Vasodilation During Heat Stress In Cystic Fibrosis
Dean L. Kellogg, Jr.1*, Gary J. Hodges2, Carlos R. Orozco3, Terri M. Phillips4, Joan Liu Zhao1, and John M. Johnson5
1 Medicine, University of Texas Health Science Center, San Antonio, Texas, United States
2 Physiology, University of Texas Health Science Center, San Antonio, Texas, United States
3 Adult Cystic Fibrosis Clinic, Christus Santa Rosa Hospital, San Antonio, Texas, United States
4 San Antonio, Texas, United States; Adult Cystic Fibrosis Clinic, Christus Santa Rosa Hospital, San Antonio, Texas, United States
5 Department of Physiology, University of Texas Health Science Center, San Antonio, Texas, United States
* To whom correspondence should be addressed. E-mail: kelloggd{at}uthscsa.edu.
To test the hypothesis that cutaneous active vasodilation in heat stress is mediated by a redundant cholinergic co-transmitter system, we examined the effects of atropine on skin blood flow (SkBF) increases during heat stress in persons with (CF) and without cystic fibrosis (non-CF). VIP has been implicated as a mediator of cutaneous vasodilation in heat stress. VIP-containing cutaneous neurons are sparse in CF, yet SkBF increases during heat stress are normal. In CF, augmented Ach release or muscarinic receptor sensitivity could compensate for decreased VIP; if so, active vasodilation would be attenuated by atropine in CF relative to non-CF. Atropine was administered into skin by iontophoresis in 7 CF and 7 matched non-CF subjects. SkBF was monitored by laser-Doppler flowmetry (LDF) at atropine treated and untreated sites. Blood pressure (MAP) was monitored (Finapres) and cutaneous vascular conductance calculated (CVC=LDF/MAP). The protocol began with a normothermic period followed by a 3 minute cold stress and 30-45 minutes of heat stress. Finally, LDF sites warmed to 42°C to effect maximal vasodilation. CVC was normalized to its site-specific maximum. During heat stress, CVC increased in both CF and non-CF (p<0.01). CVC increases were attenuated by atropine in both groups (p<0.01); however, the responses did not differ between groups (p=0.99). We conclude that in CF there is not greater dependence on redundant cholinergic mechanisms for cutaneous active vasodilation than in non-CF.
