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ISCHAEMIA ENHANCES THE ROLE OF CA2+‐ACTIVATED K+ CHANNELS IN ENDOTHELIUM‐DEPENDENT AND NITRIC OXIDE‐MEDIATED DILATATION OF THE RAT HINDQUARTERS VASCULATURE

1. We compared the effects of the nitric oxide synthase inhibitor NG‐nitro‐l‐arginine (l‐NOARG) and tetraethylammonium (TEA), a blocker of large conductance Ca2+‐activated K+ (BKCa) channels, on vasodilator responses to endothelium‐dependent (acetylcholine; ACh) and ‐independent (sodium nitroprusside; SNP) vasodilators. The mechanism of the vasodilator responses was determined in rat hindquarters under normal conditions (sham ischaemia) and after 2 h ischaemia followed by reperfusion with physiological saline.