Coronary endothelium is responsive to bradykinin and arachidonate but not to acetylcholine.

In preparations of either endothelium-rubbed or intact porcine coronary artery, in which sodium nitroprusside caused a relaxation, acetylcholine did not cause a relaxation but a contraction. Calcium ionophore A23187 and bradykinin elicited a dose-dependent relaxation in preparations with intact endothelium, while the relaxation was abolished by rubbing the endothelium. Bradykinin-induced relaxation was not inhibited by acetylsalicylic acid (10(-4) M), indomethacin (10(-6) M), and combined treatment with phentolamine (10(-6) M) and propranolol (10(-6) M). Arachidonic acid produced an endothelium-dependent contraction, which, at 10(-5) M, was followed by a slowly developing relaxation. Prostaglandin I2 caused a slight relaxation of the artery. In conclusion, endothelial cells of porcine coronary artery respond to bradykinin and A23187, presumably through a release of the endothelium-derived relaxing factor. Vasoconstrictor prostanoid(s) seem(s) to be involved in the arachidonic acid-induced contraction.