We have demonstrated previously that hypoxia and adenosine dilate pressurised human coronary resistance arteries with myogenic tone. These responses were not mediated by glibenclamide sensitive K_ATP channels¹. This study aims to assess the hypoxic and adenosine responses when a different stimulus, KCl, activates the arteries. Human coronary resistance arteries were dissected from atrial appendage obtained at the time of cardiac surgery in accord with local ethics guidelines. Vessels were mounted on a pressure myograph, pressurised to 60mmHg perfused with physiological saline solution, gassed with 95% air 5% CO₂, and checked for leaks. Lumen diameter was continually monitored using a video dimension analyzer. Arteries were stimulated with high K⁺ solution (60mM KCl isosmotically substituted for NaCl) and a stable response achieved. One group of vessels (n = 6) was subjected to a 10 minute hypoxic challenge, (< 10mmHg O₂) induced by switching to a 95% N₂/5% CO₂ gas mixture. A separate group of arteries (n=6) were also stimulated with 60mM KCl and the response to cumulative additions of adenosine (10^-8 – 10^-4M) recorded. The effect of glibenclamide, a K_ATP channel blocker, (10^-7 – 10^-5M) on the adenosine response was assessed. Mean diameter (±SEM) of arteries (n=12) used was 145 ± 15μm. 60mM KCl produced a mean constriction of 35 ± 10μm, which, in the absence of other stimuli, was stable for the period of the experiment. Hypoxia had no effect on diameter in depolarized arteries (mean change in diameter as % change to KCl = -7 ± 9%). Following return to normoxia, washout of KCl resulted in return of arterial diameter to baseline levels. Addition of adenosine resulted in dilation of depolarized arteries. This was significant for concentrations of 10^-5M (27 ± 21%) and 10^-4M (116 ± 69%) (P < 0.01, paired t test, when comparing diameters). Glibenclamide (10^-7M – 10^-5M) did not significantly alter the 10^-4M adenosine-induced dilation (117 ± 66%, 133 ±62% and 142 ± 67%) respectively. These data show that high K⁺ constricts human coronary resistance arteries. Hypoxia does not alter this constriction. This observation contrasts with our previous finding that both hypoxia dilates human coronary arteries constricted with myogenic tone¹. However higher concentrations of adenosine produce significant dilations which appear to be insensitive to K_ATP channel inhibition which agrees with our previous findings¹. These results suggest that the response of pressurised human coronary resistance arteries to hypoxia depends on the stimulus applied to the artery. When constricted with KCl adenosine ultimately dilates while hypoxia does not elicit a vasomotor response. The mechanism of these responses remains to be elucidated.