The α2C-adrenoceptor deletion322–325 variant and cold-induced vasoconstriction

Eitan A. Friedman, Paul A. Harris, Alastair J. J. Wood, C. Michael Stein, Daniel Kurnik
2009 Clinical Autonomic Research  
Objectives-Cold-induced vasoconstriction is mediated in part by selective enhancement of local α 2C -adrenoceptor (α 2C -AR) activity. A common insertion-deletion variant in the α 2C -AR gene (ADRA2C del322-325) results in an approximately 85% reduction of agonist-mediated function in vitro. We tested the hypothesis that individuals with the ADRA2C del322-325 variant have attenuated vasoconstriction in response to cold. Methods-Cutaneous digital blood flow (flux) was measured by laser Doppler
more » ... owmetry in a controlled environment at room temperature and during two cycles of graduated local heat and cold exposure in 31 subjects. Temperature-response curves were analyzed to estimate the following measures: E min (minimal flux during cooling), and ET 50 and ET 90 (the local temperature at which flux decreased by 50% and 90% respectively). Results-We found no significant genotypic differences in E min (24.3±19.5, 30.0±20.5, and 21.5 ±25.9 AU for ins/ins, ins/del, and del/del genotypes, respectively; P=0.48), ET 50 (25.5±6.0, 25.1 ±6.7, and 25.1±7.1 °C; P=0.99), or ET 90 (20.5±4.7, 22.1±4.0, and 20.8±6.7 °C; P=0.77) in either the first or second heating and cooling cycle (cycle 1 values presented). Interpretation-The ADRA2C del322-325 variant did not affect vascular sensitivity to local cold exposure.
doi:10.1007/s10286-009-0014-5 pmid:19444546 pmcid:PMC2739683 fatcat:b5ggj56ld5chfmmx34atmxq3pi