In the presence of potassium (K<sup>+</sup>), A23187 and substance P elicited endothelium-dependent relaxations of porcine coronary arteries. Isoproterenol or hypoxia elicited endothelium-independent relaxations. Rubbing the artery potentiated the contractile response to a low K<sup>+</sup> concentration (15.4 ml). After intact arteries had been stored at 5 ° C for 3 days, K<sup>+</sup>-induced maximal tension was not affected, but contractile responses to 15 mM K<sup>+</sup> were potentiated with a decrease in ED<sub>50</sub>, suggesting that cold storage produces a supersensitivity to K<sup>+</sup>. Endothelium-dependent relaxations were abolished after 3 days of cold storage, while endothelium-independent relaxations were not inhibited. Cold storage of arteries with l-arginine (1 mM) for 3 days did not alter the relaxation responses to substance P and A23187, indicating that l-arginine does not prevent the loss of endothelium-dependent relaxation. Cold storage for 5 days inhibited the maximal tension to K<sup>+</sup> and abolished the supersensitivity. Scanning electron micrographs showed that endothelial cells can be damaged by prolonged cold storage. The changes in tension response of the artery were correlated with the time course of endothelial cell loss resulting from cold storage.