Harasawa Y, Kimura M, Ohno Y, Hayashi S
Department of Pharmacology, Upjohn Tsukuba Research Laboratories, Japan.
Arch Int Pharmacodyn Ther. 1989 Nov-Dec;302:196-208.
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.
在猪冠状动脉内皮擦除或完整的标本中，硝普钠可引起血管舒张，而乙酰胆碱却不会引起舒张反而会导致收缩。钙离子载体A23187和缓激肽在完整内皮的标本中可引起剂量依赖性舒张，而擦除内皮后这种舒张作用消失。乙酰水杨酸（10⁻⁴M）、吲哚美辛（10⁻⁶M）以及酚妥拉明（10⁻⁶M）与普萘洛尔（10⁻⁶M）联合处理均不抑制缓激肽诱导的舒张。花生四烯酸产生一种内皮依赖性收缩，在10⁻⁵M时，随后会出现缓慢发展的舒张。前列环素I2可使动脉出现轻微舒张。总之，猪冠状动脉内皮细胞对缓激肽和A23187有反应，可能是通过释放内皮源性舒张因子。血管收缩性前列腺素似乎参与了花生四烯酸诱导的收缩。
