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1 Kinesiology Department, The Pennsylvania State University, University Park, Pennsylvania, United States
2 Anesthesiology and Critical Care Medicine, The Johns Hopkins University School of Medicine, Baltimore, Maryland, United States
3 Kinesiology Department, Pennsylvania State University, University Park, Pennsylvania, United States; Intercollege Graduate Degree Program in Physiology, The Pennsylvania State University, University Park, Pennsylvania, United States
* To whom correspondence should be addressed. E-mail: cthomp44{at}jhmi.edu.
Cutaneous vasoconstriction (VC) is the initial thermoregulatory response to cold exposure and can be elicited through either whole-body or localized skin cooling. However, the mechanisms governing local cold-induced VC are not well-understood. We tested the hypothesis that Rho kinase participates in local cold-induced cutaneous VC. In 7 men and women (20-27 years), up to four ventral forearm skin sites were instrumented with intradermal microdialysis fibers for localized drug delivery during cooling. Skin blood flow was monitored at each site with laser Doppler flowmetry (LDF) while local skin temperature was decreased and maintained at 24°C for 40 minutes. Cutaneous vascular conductance (CVC; LDF/mean arterial pressure) was expressed as percentage change from 34°C baseline (%
CVCbase). During the first 5 minutes of cooling, CVC decreased at control sites (lactated Ringers) to -45±6% (p<0.001), increased at adrenoceptor-antagonized sites (yohimbine+propranolol) to 15±14% (p=0.002), and remained unchanged at both Rho kinase-inhibited (fasudil) and adrenoceptor-antagonized+Rho kinase-inhibited sites (yohimbine+propranolol+fasudil) (-9±1%, p=0.4 and -6±2%, p=0.4, respectively). During the last 5 minutes of cooling, CVC further decreased at all sites compared to baseline values (control:-77±4%, p<0.001; adrenoceptor-antagonized: -61±3%, p<0.001; Rho kinase-inhibited: -34±7, p<0.001; and adrenoceptor-antagonized+Rho kinase-inhibited: -35±3%, p<0.001). Rho kinase-inhibited and combined treatment sites were significantly attenuated compared to both adrenoceptor-antagonized (p<0.01) and control sites (p<0.0001). Rho kinase mediates both early- and late-phase cold-induced VC, supporting in vitro findings and providing a putative mechanism through which both adrenergic and non-adrenergic cold-induced VC occurs in an in vivo human thermoregulatory model.
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