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No direct role for A1/A2 adenosine receptor activation to reflex cutaneous vasodilatation during whole-body heat stress in humans


Correspondence: B. J. Wong, PhD, Department of Kinesiology, 1A Natatorium, Kansas State University, Manhattan, KS 66506, USA.




The precise mechanisms underlying reflex cutaneous vasodilatation during hyperthermia remain unresolved. The purpose of this study was to investigate a potential contribution of adenosine A1/A2 receptor activation to reflex cutaneous vasodilatation.


Eight subjects were equipped with four microdialysis fibres on the left forearm, and each fibre was randomly assigned one of four treatments: (1) lactated Ringer's (control); (2) 4 mm of the non-selective A1/A2 adenosine receptor antagonist theophylline; (3) 10 mm L-NAME to inhibit nitric oxide (NO) synthase; and (4) combined 4 mm theophylline and 10 mm L-NAME. Laser-Doppler flowmetry (LDF) was used as an index of skin blood flow, and blood pressure was measured beat-by-beat via photoplethysmography and verified via brachial auscultation. Whole-body heat stress to raise oral temperature 0.8 °C above baseline was induced via water-perused suits. Cutaneous vascular conductance (CVC) was calculated as LDF/mean arterial pressure and normalized to maximal (%CVC max) via infusion of 28 mm nitroprusside and local heating to 43 °C.


There was no difference between control (65 ± 5%CVC max) and theophylline (63 ± 5%CVC max) sites. L-NAME (44 ± 4%CVC max) and theophylline + L-NAME (32 ± 3%CVC max) sites were significantly attenuated compared to both control and theophylline only sites (P < 0.05), and combined theophylline + L-NAME sites were significantly reduced compared to L-NAME only sites (P < 0.05).


These data suggest A1/A2 adenosine receptor activation does not directly contribute to cutaneous active vasodilatation; however, a role for A1/A2 adenosine receptor activation is unmasked when NO synthase is inhibited.