We have previously reported that noradrenaline (NAd) inhibited mouse colonic motility via the α1A adrenergic receptor (α1A AR)-small conductance Ca²⁺-activated K⁺ (SK) channel signal pathway in PDGFRα⁺ cells. In the present study, we studied the effects of NAd and pituitary adenylate cyclase-activating polypeptide (PACAP) on contractile and electrical activities of circular smooth muscle cells (CSMCs) in the human colon. NAd inhibited colonic contractions through binding to α1A AR. PACAP and maxadilan, a PACAP type 1 receptor (PAC1) agonist, also inhibited colonic contractions. The inhibitory effects of these drugs were sensitive to apamin, a blocker of SK channel. However, the latency of the responses to PACAP or maxadilan were significantly longer than NAd. Similar latency of the responses was also observed when we recorded apamin-sensitive membrane hyperpolarization evoked by NAd and maxadilan in colonic CSMCs intracellularly. These results suggest that PDGFRα⁺ cells integrate inhibitory inputs from NAd and PACAP, leading to the activation of G protein coupled receptor-SK channel signal pathway in the human colon. NAd and PACAP may work together with different inhibitory time course to regulate colonic contractility during sustained stress.