Objectives
Cold-induced vasoconstriction is mediated in part by selective enhancement of local α2C-adrenoceptor (α2C-AR) activity. A common insertion–deletion variant in the α2C-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 flowmetry 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 ET50 and ET90 (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), ET50 (25.5 ± 6.0, 25.1 ± 6.7, and 25.1 ± 7.1°C; P = 0.99), or ET90 (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.