Asthma and other airway diseases are often classified by symptoms that include airway hyperresponsiveness (AHR), the excessive contraction of airway smooth muscle cells (ASMCs) in response to a variety of stimuli. The hypercontraction of ASMCs may result from membrane depolarization followed by activation of voltage‐sensitive Ca2+ channels (VSCCs). K+ channels have a high open probability in the absence of ASMC hypercontraction and therefore are thought to oppose membrane depolarization. Using image analysis techniques to measure airway constriction in rat precision cut lung slices (PCLS), we found that blocking voltage‐activated K+ channels using 2mM 4‐aminopyridine (4‐AP) resulted in only 6.3 % constriction of rat airways whereas 230nM methacholine (MeCh) gave rise to 41% constriction. Both responses were blocked by 10μM verapamil. We hypothesized that in the presence of MeCh, K+ channel blockers would cause amplified constriction of the airways when compared to MeCh alone. However, on average, we found that blocking voltage‐gated K+ channels using 2mM 4‐AP in the presence of 230nM MeCh caused significantly less constriction than with MeCh alone in rat PCLS. These findings suggest that Kv channel activity is essential for optimal MeCh‐induced bronchoconstriction. Further work is required to elucidate the roles of Kv channels in bronchoconstriction. (Research supported by Loyola University Chicago.)